Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

M1 - Immuno > Exam 2 Material > Flashcards

Exam 2 Material Flashcards

1
Q

what is the major mechanism by which the immune system kills both tumor cells and the cells of tissue transplants ?

A

CD8+ cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

immune surveillance

A

immune system usually recognizes and eliminates neoplastic/malignant cells before they start proliferating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

why are tumors often able to survive and grow in otherwise immunocompetent individuals?

A

tumor immunity is often incapable of preventing tumor growth or is easily overwhelmed by rapidly growing tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what evidence exists that tumor responses against tumors inhibit tumor growth?

A

lymphocytic infiltrates around some tumors and enlargement of draining lymph nodes correlate with better prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what evidence exists that tumor recognition shows features of adaptive immunity and is mediated by lymphocytes?

A
  • tumor transplants are rejected by animals (and more rapidly if previously exposed)
  • immunity to tumor transplants can be transferred by lymphocyte transfer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what evidence exists that the immune system protects against tumor growth?

A

immunodeficient people have higher incidence of some tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what evidence exists that tumors evade surveillance in part by activating inhibitory receptors on T cells?

A

theraputic blockade of inhibitory receptors (CTLA-4, PD-1) can lead to tumor remission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

5 features of immune response to tumors

A
  1. immune system protects against tumor growth
  2. tumor recognition shows features of adaptive immunity
  3. tumor recognition is mediated by lymphocytes
  4. tumor responses against tumors inhibit tumor growth
  5. tumors evade surveillance in part by activating inhibitory receptors on T cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what must a tumor do to be recognized by immune system?

A

must express antigens that are seen as non-self

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

5 types of tumor antigens may be recognized by the immune system

A
  1. mutated self protein that does not contribute to tumorigenesis
  2. product of oncogene
  3. product of mutated tumor suppressor gene
  4. overexpressed/aberrantly expressed self-protein
  5. oncogenic virus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

examples of mutated self proteins that do not contribute to tumorigenesis

A

various mutant proteins in carcinogen or radiation-induced tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

examples of products of oncogenes

A

mutated Ras; Bcr/Abl fusion proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

examples of overexpressed/aberrantly expressed self-proteins

A

tyrosinase; gp100; cancer/testis antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are some examples of oncogenic viruses?

A

HPV E6; cervical carcinoma E7 proteins; EBV-induced lymphoma EBNA proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

driver mutations

A

products of mutated or translocated oncogenes or tumor suppressor genes that presumably are involved in the process of malignant transformation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

when can structurally normal self-proteins elicit immune responses?

A

when they are aberrantly expressed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

characteristic of majority of tumor antigens that elicit immune responses

A

endogenously-synthesized cytosolic or nuclear proteins displayed as Class I MHC-associated peptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

how are cytotoxic T cell responses against tumors induced?

A

recognition of tumor antigens on APCs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

from what types of cells can tumors arise?

A

virtually any nucleated cell (b/c they express MHC I)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

3 phases of immune surveillance / tumor growth

A
  1. Elimination (immune surveillance)
  2. Equilibrium (immunoediting)
  3. Escape
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

immunoediting

A

variant tumor cells arise that are more resistant to being killed; over time, a variety of tumor variants develop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Clinical example of equilibrium phase?

A

woman treated for malignant melanoma 16 yrs before death; both kidneys donated to recipients who developed melanoma 1-2 years later (remember, transplant recipients are immunosuppressed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

3 immunotherapy options for tumors

A
  1. passive immunity through transfer of tumor-specific T cells or antibodies
  2. active T cell immunity enhanced by vaccination with tumor antigen-pulsed dendritic cell
  3. active immunity enhanced by blocking inhibitory T cell receptors (CTLA-4, PD-1)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

immunodiagnostics

A
  • Identification of cell of origin of an undifferentiated tumor
  • Monitoring serum levels of cancer markers during treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

cancer vaccine ideas

A
  • heat shock proteins (clinical trials)
  • genetic modifications of tumor cells
  • creation of dendritic cell-tumor cell hybrid (hybridoma) – do NOT have to know tumor Ag
  • recombinant IFN-alpha (renal cell carcinoma, melanoma)
  • IL-2 adoptive cellular therapy (didn’t work)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

cross-presentation

A

dendritic cell activates naive CD8+ T cell specific for antigens of a virus-infected or tumor cell that it has ingested by presenting the antigen to the T cell AND providing costimulation; also called cross-priming

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

problems with antibody-directed therapy

A
  • tumor heterogeneity (some cells may not express the right antigen)
  • low density of tumor antigen expression
  • modulation of tumor antigen levels
  • antibodies must bind to every tumor cell to kill it (no bystander killing)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

ADEPT

A

antibody-directed enzyme/pro-drug therapy; monoclonal antibody-enzyme conjugate – nontoxic pro-drug given and metabolized to active drug to produce high concentrations of cytotoxic drug localized at tumor site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

why do immune responses often fail to check tumor growth?

A

tumors evolve in the host to evade immune recognition or resist immune effector mechanisms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

6 mechanisms of tumor cell resistance to immune recognition and destruction

A
  1. tumor stops expressing recognized antigen (antigen loss variants)
  2. tumor stops expressing class I MHC
  3. tumor secretes cytokines that suppress immune responses (ex: TGF-β)
  4. tumor expresses ligands for T cell inhibitory receptors (ex: PD-1)
  5. tumor induces regulatory T cells, which suppress CD4/CD8 effector
  6. tumor induces low levels of B7 costimulators on APCs → preferential engagement of inhibitory receptor (CTLA-4) on T cells rather than stimulatory receptor (CD28)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

major hallmark of cancer

A

ability to avoid destruction by the immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what activates NK cells?

A

lack of MHC class I expression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

CTLA-4

A

up-regulated during T cell activation; high affinity for B7; inhibits activated T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

main strategies/goals for cancer immunotherapy

A
  • provide anti-tumor effectors (antibodies / T cells)
  • actively immunize patients against their tumors
  • stimulate patients’ own anti-tumor immune responses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

problems with chemotherapy / radiation treatment of tumors

A

damage normal non-tumor tissues; associated with serious toxicities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

antibody specific for CD20 used to treat…?

A

B cell tumors (usually along with chemotherapy); CD20 is not expressed by hematopoietic stem cells, so normal B cells are replenished after antibody treatment is stopped

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

dendreons provenge vaccine

A

for advanced prostate cancer; extended life expectancy ~4mos; few side effects; super expensive; company filed for bankruptcy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

3 ways antibody treatment could generally help destroy a tumor

A
  1. antibodies could bind to tumor antigens and either activate host effector mechanisms, such as phagocytes or the complement system, or deliver toxins to the tumor cells
  2. antibodies could block growth factor signaling (ex: Her2/Neu in breast cancer)
  3. antibodies could inhibit angiogenesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

adoptive cellular immunotherapy

A

T cells isolated from blood or tumor infiltrates of a patient, expanded with growth factors, and injected back into the same patient. The T cells presumably contain tumor-specific CTLs, which find the tumor and destroy it. (Variable results so far.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

example of mutated tumor suppressor gene

A

mutated p53

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

PD-1

A

inhibits T cells (like CTLA-4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

PD-L1/2

A

inhibitory ligand for PD-1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

immune system “backup” for tumor cells that evade CD8+ cells?

A

NK cells – especially important when tumor cells don’t express MHC I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

tumor microenvironment

A

disrupts CD3 signaling complex (zeta or epsilon chain)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

TAM

A

tumor-associated macrophage; tumor promotes class-switching from M1 to M2, which induces angiogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

equilibrium phase of tumor cells

A

tumor cells that can evade the immune system arise and develop; Treg cells recruited

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

escape phase of tumor cells

A

tumor cell has successfully evaded immune system and begins to spread/proliferate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

mice without gamma-delta T cells

A

develop skin cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

mice without RAG and STAT1

A

increased incidence of gut and breast tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

antibodies against CD20

A

can be used to kill B cell tumors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

block CTLA-4 or PD-1

A

prevent T cell inactivation and hopefully kill tumor cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what could kill a tumor that does not express MHC Class I?

A

NK cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

genes that contribute the most to the rejection of grafts

A

MHC genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

syngeneic grafts

A

from an identical member of a species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

allogeneic grafts

A

from a different member of a species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

xenogeneic grafts

A

from a different species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

which grafts are always rejected by a recipient with a normal immune system?

A

allografts and xenografts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

antigens of allografts that serve as principal targets of rejection?

A

proteins encoded in MHC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

human MHC

A

HLA complex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

MHC Class I corresponds to which HLAs?

A

HLA-A, -B, and -C

*remember, Class I – CD8!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

MHC Class II corresponds to which HLAs?

A

HLA-DQ, -DP and -DR

*remember, Class II – CD4!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

one of the strongest immune responses known?

A

response to MHC antigens on another individual’s cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

example of immunologic cross-reaction?

A

T cell recognition of allogeneic MHC molecules in allografts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

why do T cells recognize allogeneic molecules?

A
  • Allogeneic MHC molecules containing peptides derived from allogeneic cells may look like self-MHC molecules with bound foreign peptides
  • a single allogeneic graft cell will express thousands of MHC molecules, every one of which may be recognized as foreign by a graft recipient’s T cells
  • there is no mechanism for selectively eliminating T cells whose TCRs have a high affinity for allogeneic MHC molecules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

how many T cells may react against an allogeneic molecule?

A

0.1% to 1% of all T cells (compared to 1 in 10^5 or 10^6 T cells that recognize any microbial antigen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

minor histocompatibility antigens

A

Non-MHC antigens that induce graft rejection (though usually not as strongly); most are allelic forms of normal cellular proteins that happen to differ between donor and recipient; important in blood transfusions and hematopoietic stem cell transplantation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

direct allorecognition

A

T cells in the recipient recognize unprocessed donor allogeneic MHC molecules on graft dendritic cells; stimulates CTLs that attack graft

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

indirect allorecognition

A

graft cells (or alloantigens) are ingested by recipient dendritic cells; donor alloantigens are processed and presented by self-MHC molecules on recipient APCs to T cells; alloreactiv CD4+ cells (rather than CTLs) attack graft

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

CTLs attack graft in what kind of recognition?

A

direct allorecognition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

CD4+ cells attack graft in what kind of recognition?

A

indirect allorecognition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

mixed lymphocyte reaction

A

in vitro model of T cell recognition of alloantigens – T cells from one individual are cultured with leukocytes of another individual, and T cell responses are assayed; magnitude of response is proportional to the extent of MHC differences btwn these individuals and is a rough predictor of the outcomes of grafts exchanged between these individuals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

alloantibodies

A

also contribute to graft rejection; most are helper T cell–dependent high-affinity antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

alloantibody production

A

recipient B cells recognize donor alloantigens and then process and present peptides derived from these antigens to helper T cells (that may have been previously activated by recipient DCs presenting the same donor alloantigen), thus initiating antibody production. (This is a good example of indirect presentation of alloantigens)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

hyperacute rejection

A

occurs w/i minutes of transplantation; characterized by thrombosis of graft vessels and ischemic necrosis of graft; mediated by antibodies that bind to antigens on the graft vascular endothelium and activate the complement and clotting systems, leading to injury to endothelium and thrombus formation; major barrier to xenotransplantation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

acute rejection

A

occurs within days or weeks after transplantation; due to active immune response of host stimulated by alloantigens in graft; mediated by T cells (CD4+ or CD8+) and antibodies; the principal cause of early graft failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

chronic rejection

A

occurs over months or years, leading to progressive loss of graft function; may be manifested as graft fibrosis and graft arteriosclerosis; culprits believed to be T cells that react against graft alloantigens and secrete cytokines that stimulate the proliferation and activities of fibroblasts and vascular smooth muscle cells; alloantibodies also contribute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

most common complication associated with organ transplant survivability?

A

chronic rejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

current immunosuppressive therapy designed primarily to prevent what?

A

acute rejection (activation of alloreactive T cells)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

therapeutic monoclonal therapy with an anti-CD25 agent is most similar to which drug therapy?

A

Rapamycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

principal cause of graft failure?

A

chronic rejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

mainstay of preventing and treating the rejection of organ transplants?

A

immunosuppression, primarily of T cell activation and effector functions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

cyclosporine / tacrolimus

A

block T cell cytokine production by inhibiting calcineurin activation of NFAT; very effective in preventing graft/transplant rejection (compared to Azathioprine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

rapamycin

A

blocks lymphocyte (T and B cell) proliferation by inhibiting mTOR and IL-2 signaling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

mTOR

A

required for T cell responses to cytokine growth factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

major problem with immunosuppressive drugs?

A

nonspecific immunosuppression – inhibit immune responses to more than just the graft

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

MHC matching

A

critical for the success of transplantation of some types of tissues (allogeneic bone marrow grafts) and improves survival of other types of organ grafts (renal allografts), BUT modern immunosuppression is so effective that HLA matching is not considered necessary for many types of organ transplants (heart), especially b/c # of donors is limited and recipients often are too sick to wait for well-matched organs to become available

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

long-term goal of transplant immunologists?

A

induce immunological tolerance specifically for the graft alloantigens – will allow graft acceptance without shutting off other immune responses in the host

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Xenotransplantation

A

possible solution for problem of shortage of suitable donor organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

frequent cause of xenotransplant loss?

A

hyperacute rejection b/c individuals often contain “natural” antibodies that react with cells from other species and the xenograft cells lack regulatory proteins that can inhibit human complement activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

natural antibodies

A

mediate hyperacute rejection of xenografts; production does not require prior exposure to the xenoantigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

transfusion

A

Transplantation of circulating blood cells, platelets, or plasma from one individual to another

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

major barrier to transfusion

A

presence of foreign blood group antigens, the prototypes of which are the ABO antigens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

ABO antigens

A

carbohydrates on membrane glycoproteins or glycosphingolipids; contain a core glycan that may have an additional terminal sugar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

transfusion reaction

A

Immunologic reaction against transfused blood products, usually mediated by preformed antibodies in the recipient that bind to donor blood cell antigens, such as ABO blood group antigens or histocompatibility antigens. Transfusion reactions can lead to intravascular lysis of red blood cells and, in severe cases, kidney damage, fever, shock, and disseminated intravascular coagulation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Rh antigen

A

Rhesus factor; red cell membrane protein that can be the target of maternal antibodies that may attack a developing fetus when the fetus expresses paternal Rh and the mother lacks the protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Blood type A

A

N-acetylgalactosamine terminal sugar; makes anti-B antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Blood type B

A

galactose terminal sugar; makes anti-A antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Blood type AB

A

N-acetylgalactosamine AND galactose terminal sugars; no antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Blood type O

A

no terminal sugars – only core glycan; makes both anti-A and anti-B antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Hematopoietic stem cell transplantation

A

bone marrow cells or, more often, hematopoietic stem cells mobilized in a donor’s blood are injected into the circulation of a recipient, and the cells home to the marrow; used increasingly to correct hematopoietic defects, to restore bone marrow cells damaged by irradiation and chemotherapy for cancer, and to treat leukemias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Hematopoietic stem cell transplantation problems

A
  • Before transplantation, some of the recipient’s bone marrow has to be destroyed to create space to receive the transplanted stem cells, and this inevitably causes deficiency of blood cells, including immune cells
  • The immune system reacts strongly against allogeneic hematopoietic stem cells, so successful transplantation requires careful HLA matching of donor and recipient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

graft-vs-host disease

A

if mature allogeneic T cells are transplanted with the stem cells, these mature T cells can attack the recipient’s tissues and cause a systemic inflammatory reaction characterized by rashes, diarrhea, liver disease, eosinophilia, and enlarged lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

main factor dictating graft survival?

A

MHC compatibility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Maternal Tolerance to Fetal Tissues

A

fetus expresses paternal alloantigens but is not rejected by mother; trophoblast and placenta play key role in tolerance but mechanisms unclear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Graft-vs-Leukemia Effect

A

mature T cells can kill leukemia cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

mycophenolate mofetil

A

blocks lymphocyte proliferation by inhibiting guanine nucleotide (DNA) synthesis in lymphocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

corticosteroids

A

reduce inflammation; adverse effects include fluid retention, weight gain, diabetes, bone loss, skin thinning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

antithyomcyte globulin

A

binds to and depletes T cells by promoting phagocytosis or complement-mediated lysis; used to treat acute rejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

anti-IL-2 (CD25) receptor antibody

A

inhibits T cell proliferation by blocking IL-2 binding; may also opsonize and help eliminate activated T cells that express IL-2R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

CTLA-4-Ig (belatacept)

A

inhibits T cell activation by blocking B7 costimulator binding to CD28

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

anti-CD52 (alemtuzumab)

A

depletes lymphocytes by complement-mediated lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

antibody-directed immunotherapy

A

inject monoclonal antibodies against tumor antigens or against signaling molecules (i.e. T cell inactivators); can combine with a toxin or radioactive molecule to try to directly kill tumor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

antibody-directed enzyme/pro-drug therapy (ADEPT)

A

antibody conjugated with enzyme; antibody-enzyme complex binds target cell; nontoxic pro-drug given, which antibody-enzyme complex cleaves into active form at the tumor site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

CSF1/CSF1R Blockade

A

Reprograms Tumor-Infiltrating Macrophages and Improves Response to T Cell Checkpoint Immunotherapy in Pancreatic Cancer Models

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

ways to improve efficacy of anti-tumor antibodies

A
  1. Humanize antibodies-make mouse Abs more human
  2. Smaller Abs
  3. Make bi-functional antibodies or fusion proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

-Omab

A

fully mouse antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

-Ximab

A

chimeric antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

-Zumab

A

humanized antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

-Umab

A

fully human antibody

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Ipilimumab

A

human antibody directed against CTLA-4; used for metastatic melanomas; very expensive but very effective (pts survive avg 6-9mos, sometimes longer); tumor cells remain in equilibrium phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

existing cancer vaccine?

A

HPV-16; does not eliminate established tumors but can prevent infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

generating specific anti-tumor T cells

A

Adoptive T cell immunotherapy; viral vector used to recombine T cell alpha and beta chain genes with specific vector DNA; viral particles infect other T cells and cause them to express these genes; T cells become specific for tumor and attack it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Chimeric Antigen Receptor (CAR)–Modified T Cells

A

anti-CD19/CD137 (costimulatory receptor) / CD3zeta (signal transduction) CAR–modified T cells re-infused into a patient expanded 1000 fold; chimeric T cells still detectable 6 months after infusion; regression of axillary lymphadenopathy occurred within 1 month after infusion and was sustained; B cell lymphopenia is complication but can be managed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

3 stages of tumor development

A
  1. elimination / immune surveillance
  2. equilibrium / immunoediting
  3. escape
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Adoptive T cell immunotherapy

A

infuses the patient’s modified TCR (CAR) lymphocytes using CD3 antibody and IL-2; efficacy due to robust clonal expansion of infused cells, resulting in destruction of tumor and development of anti-tumor memory cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

most promising immunotherapy to combat already established tumors?

A

Generation of anti-tumor T cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

“Second Set” Graft

A

introducing 2nd graft from same donor to same recipient; can show that exposure to 1st graft created immunological memory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

graft rejection requires what type of lymphocytes?

A

T cells – depletion or inactivation of T cells leads to reduced graft rejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

graft rejection is mediated by what cells?

A

lymphocytes – the ability to reject a graft rapidly can be transferred to a naive individual through lymphocytes from a sensitized individual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

graft rejection shows which 2 cardinal features of adaptive immunity?

A

memory and specificity – prior exposure to donor MHC molecules leads to accelerated graft rejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

how to mitigate cytotoxic effects of steroids?

A

lower doses of steroids + other immunosuppressive drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Anti-metabolites

A

originally used to treat cancer but now used in post-transplantation therapy; includes Azathioprine, Cyclophosphamide, Mycophenolate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Azathioprine

A

purine analog that interferes with DNA synthesis; cytotoxic to T & B cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Cyclophosphamide

A

alkylating agent; used in chemical weapons (nitrogen mustard)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Immunosuppressors that interfere with T cell signaling

A

Cyclosporin/Tacrolimus, Rapamycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

why does matching HLA between donor and recipient not prevent organ rejection?

A

multiple minor histocompatibility loci differences

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

what kinds of transplants are most likely to cause graft-vs-host disease?

A

Hematopoietic stem cell transplants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Type I Hypersensitivity

A

immediate; Th2, IgE, mast cells, eosinophils; allergy/atopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Hypersensitivity

A

excessive or aberrant immune response causing injury or pathology to tissues of the body; can be:

1) dysregulated / uncontrolled response to foreign antigen causing damage
2) aberrant response against self – “autoimmunity “

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

allergy

A

Disorder caused by an immediate hypersensitivity reaction, often referring to the type of antigen that elicits the disease, such as food allergy, bee sting allergy, and penicillin allergy. All these conditions are the result of antigen-induced TH2 generation and IgE production, and mast cell or basophil activation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Hypersensitivity reaction classification

A

classified on the basis of the principal immunologic mechanism that is responsible for tissue injury and disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

atopy

A

Propensity of an individual to produce IgE antibodies in response to various environmental antigens and to develop strong immediate hypersensitivity (allergic) responses. People who have allergies to environmental antigens, such as pollen or house dust, are said to be atopic.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

development of immediate hypersensitivity reaction

A
  • Th2 cells activated, produce IL-4 and IL-13
  • B cells stimulated to produce IgE
  • IgE binds to FceRI on mast cells
  • multiple receptors cross-linked
  • mast cell degranulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

sensitization

A

“first exposure” to an allergen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

2 phases of immediate hypersensitivity reaction

A

1) immediate phase

2) late phase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

immediate phase of immediate hypersensitivity reactions

A

develops within minutes of exposure; characterized by the release of preformed granules from the mast cell, mainly proteases and vasoactive amines (histamine), which promote vasodilation and smooth mm contraction. Over a slightly longer period of time, prostaglandins and leukotrienes also produce vasodilation and smooth mm contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

histamine

A

released by mast cells in immediate hypersensitivity reactions; promotes vasodilation, increase in vascular permeability, and smooth mm contraction; does NOT play a role in bronchial constriction / asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

late phase of immediate hypersensitivity reactions

A

develops 2-24 hours after exposure; activation of cytokine genes such as TNF that promote the recruitment of neutrophils and eosinophils that liberate proteases; primarily responsible for the tissue damage seen with repeat exposures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

major mediator of a type I hypersensitivity reaction

A

mast cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

Mast cell degranulation

A

activated by crosslinking of the FcεRI leading to release of the preformed mediators; responsible for type I hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

How an antigen or allergen affects the body and the extent of the response it stimulates depends on?

A

where antigen contacts immune system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

systemic anaphylaxis

A
  • Type I hypersensitivity
  • drugs, venom, food, serum
  • intravenous entry
  • edema, increased vascular permeability, laryngeal edema, circulatory collapse, death
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

acute urticaria (wheal-and-flare)

A
  • Type I hypersensitivity
  • animal hair, insect bites, allergy testing
  • entry through skin or systemic
  • local increase in vascular permeability & blood flow, edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

seasonal allergies

A
  • Type I hypersensitivity
  • pollens, dust mite feces
  • entry through contact with conjunctiva of eye, nasal mucosa
  • edema of conjunctiva and nasal mucosa, sneezing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

asthma

A
  • Type I hypersensitivity
  • dander, pollen, dust mite feces
  • inhalation leading to contact with mucosal lining of lower airways
  • bronchial constriction, increased mucus production, airway inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

food allergy

A
  • Type I hypersensitivity
  • nuts, shellfish, milk, eggs, soy, wheat, etc
  • oral entry
  • vomiting, diarrhea, pruritis, urticaria, anaphylaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

dendritic cells secrete what to promote Th2 differentiation?

A

IL-4, IL-5, IL-9, IL-13

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Th2 cells secrete what to perform effector functions?

A

IL-4 (germinal center rxn), IL-5 (eosinophils), IL-13 (mucus production)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

how could you inhibit allergic rxn?

A
  • inhibit the CD-40 receptor or ligand necessary for B cell activation
  • inhibit IL-4 or IL-13 which promote class switching to IgE
  • inhibit transcription factor STAT6, which promotes differentiation of Th2 cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

unique features of mast cells that make them ideally suited to mediate allergic rxns

A
  • location in epithelia – can recruit pathogen-specific lymphocytes and nonspecific effectors to sites where pathogens most often enter body
  • can promote mm contraction through lipid mediators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

mast cells secrete what?

A
  • enzymes (tryptase, chymase)
  • toxic mediators (histamine, heparin)
  • cytokines (IL-4, IL-13 [Th2]; IL-3, IL-5, GM-CSF [eosinophils]; TNF-alpha [inflammation])
  • chemokines (CCL3 – monocytes, macrophages, neutrophils)
  • lipid mediators (prostaglandins, leukotrienes [smooth mm contraction, vascular permeability, bronchoconstriction]; platelet-activating factor [attract leukocytes, activate neutrophils/eosinophils])
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

eosinophils

A

extremely cytotoxic granules great for fighting parasites, but can also cause tissue damage; multiple levels of regulation; after initial exposure to cytokines, threshold for degranulation drops, leading to development of allergic rxns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

eosinophil regulation

A
  • bone marrow produces very few
  • require eotaxins (2nd signal) to activate & allow entry into tissues
  • FcεRI not expressed constitutively, but upregulated when eosinophil activated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

chronic airway inflammation

A

can be caused by chronic Th2 activation / response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

Airway remodeling

A

hypertrophy of smooth muscle cells leads to thickened airway walls –> fibrosis from chronic asthma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

clinical pathological triad of chronic bronchial asthma

A

1) Intermittent airway obstruction
2) Chronic bronchial inflammation w/eosinophils
3) Bronchial muscle hyper-reactivity to bronchoconstrictors (cold air, exercise, viral infections, pollutants)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

treatment of anaphylaxis

A

epinephrine – vascular smooth mm contraction, increased cardiac output, bronchodilation, inhibition of mast cell degranulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

treatment of chronic bronchial asthma

A

corticosteroids, leukotriene antagonists, phosphodiesterase inhibitors – reduce inflammation, relax bronchial smooth mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

allergic disease treatment

A

1) desensitization – inject w/small doses of allergen over time to induce tolerance
2) anti-IgE antibody
3) antihistamines
4) cromolyn – inhibit mast cell degranulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

role of histamine in airway constriction?

A

none – no antihistamines for asthma treatment!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

KDPI

A

Kidney Donor Profile Index – Clinical formula incorporating 10 donor factors affecting estimated graft survival

172
Q

EPTS

A

Estimated Post-Transplant Survival

173
Q

solid organ transplants

A 
Kidney
Pancreas
Heart
Lung
Liver
Small bowel
174
Q

Quasi-tolerant state

A

the reality of organ transplantation; pharmacologically engineered; allows successful organ transplant, graft longevity, and enhanced quality of life for patients

175
Q

treatment for acute rejection

A 
High dose steroids
Thymoglobulin
Plasma exchange/IVIG
Rituximab
Bortezomib
176
Q

treatment for chronic rejection

A

Adjust and /or change immunosuppression
Control any risk factors
Re-transplantation

177
Q

Lymphoproliferative Disease

A
  • EBV related- Primary vs reactivation (B cell)
  • Related to intensity of immunosuppression
  • Acute illness (infectious mononucleosis)
  • Single or multiple tumors (LN, GI, CNS)
  • Allograft dysfunction
  • Fulminant disease
178
Q

one of the most significant technological advances in immunology and medicine?

A

Monoclonal antibodies

179
Q

Monoclonal antibodies

A

detect only one epitope on the antigen

180
Q

Polyclonal antibodies

A

recognize multiple epitopes on any one antigen; serum will contain a heterogeneous complex mixture of antibodies of different affinity

181
Q

Hemagglutination

A

a specific type of agglutination (clumping) that involves red blood cells exposed to their blood type antibody

182
Q

monoclonal antibody drugs

A

block targeted molecule functions (e.g. prevent TNF-α from binding to its receptor in the treatment of rheumatoid arthritis), modulate signaling pathways, or induce apoptosis of targeted cells

183
Q

how to make monoclonal antibodies in lab?

A
  1. Inject mouse w/antigen you want antibody to be specific for
  2. Mouse creates splenic B cells that produce antibody specific to antigen; cells isolated.
  3. Fuse cells to an immortal myeloma cell line that can’t grow in the selection medium. The only cell that can survive are fusions btwn antibody-producing B cell and myeloma cells
  4. Screen fusion cells for specific antibody you want to target by exposing them to antigen; expand cell line that is producing antibody you want
184
Q

what Ig isotype are ABO blood groups?

A

IgM

185
Q

Acute intravascular hemolytic transfusion

A

incorrect transfusion – classical pathway of complement activated when IgM binds to ABO and causes hemolysis of the recipient’s RBCs

186
Q

two blood tests that can check for antibodies that attack red blood cells?

A

Direct Coombs test and Indirect Coombs test

187
Q

Direct Coombs test

A

used to detect presence of IgG antibodies/complement proteins bound to the surface of RBCs

  • Patient’s blood sampled and serum washed away, leaving RBCs and bound antibody/complement proteins
  • Anti-IgG and Anti-complement andibodies added, which bind to Fc region of IgG or to complement, causing agglutination
  • Agglutination = positive test result
188
Q

Indirect Coombs test

A

used to detect presence of anti-RBC antibodies in plasma

  • Patient’s blood sampled and spun down to isolate serum
  • Rh+ RBCs added to serum, which bind to anti-Rh antibody in serum and form antibody-antigen complexes.
  • Anti-IgG antibodies added, which bind to Fc region of anti-Rh antibody.
  • Agglutination = positive test result
189
Q

ELISA

A

Enzyme-linked immunoabsorbant assay; used to measure specific antigen levels or antibody levels (titer) against a specific antigen

190
Q

Direct ELISA

A

used to detect specific antigens bound to a well – single enzyme-linked antibody bound to the antigen of interest

191
Q

Indirect ELISA

A

used to determine the amount of antibody in a sample – use of a primary AND secondary antibody for detection of an antibody of interest

192
Q

ELISA acute values

A

antibody levels while body is fighting the disease process

193
Q

ELISA convalescent values

A

antibody levels while body is recovering from the disease process

194
Q

difference between acute and convalescent readings to indicate a recent exposure?

A

at least 4-fold difference

195
Q

Acute ELISA is at least 4x higher than the Convalescent ELISA

A

This individual was previously exposed to the antigen and was recently exposed; his high acute response was due to the fast response by memory cells.

196
Q

Convalescent ELISA is at least 4x higher than the Acute ELISA

A

This individual was initially naïve but was recently exposed to the antigen. High convalescent is due to the gradual accumulation of antibody.

197
Q

Acute and Convalescent ELISA readings present but no significant difference

A

This individual was previously exposed but not exposed the second time. He has baseline antibody in his serum that was not elevated due to lack of new exposure to antigen.

198
Q

Western Blot

A

HIV testing; used to detect the presence of specific proteins/antibody in a sample; not as good as ELISA at quantitating the amount of antibody in a sample, but is more specific and used to confirm ELISA results

199
Q

Flow cytometry

A

uses lasers to count and sort cells in a sample by size, shape, and complexity; can also be used to detect presence of fluorescent molecules both on the cell surface and inside the cell; helps calculate relative levels or percentage of each cell type in a given sample, which is reported with a blood test with the absolute levels of
each cell type

200
Q

FACS

A

Fluorescence-activated cell sorting; specific type of flow cytometry that helps sort samples into separate containers depending on the light scattering and fluorescent characteristics of each cell.

201
Q

Lymphocyte proliferation assay

A

involves stimulating proliferation of lymphoblasts with a mitogen (e.g. pokeweed) and looking at how successfully they are able to proliferate; often done using flow cytometry; can be used to evaluate both T and B cell immunodeficiencies like SCID, DiGeorge Syndrome, Ataxia Telangietasia, etc. and to evaluate the effectiveness of T cell recovery after a transplant

202
Q

what Ig isotype are Rh antibodies?

A

IgG

203
Q

what test would you use to determine if Rh+ baby from Rh- mom?

A

direct coombs test

204
Q

what test would you use to determine if Rh- mom producing Rh antibody?

A

indirect coombs test

205
Q

what test would you use to detect HIV antibodies in serum?

A

indirect ELISA

206
Q

what test would you use to detect HIV antigen in serum?

A

direct ELISA

207
Q

Type II Hypersensitivity

A

leads to tissue injury by autoantibodies binding self-antigens, causing recruitment of complement factors and leukocytes (neutrophils!) to opsonize/destroy/phagocytose otherwise healthy, normal cells; occurs hours to a few days after initial challenge from antigen

208
Q

Type III Hypersensitivity

A

antibodies bind persistent soluble antigens to form immune complexes that are deposited mainly in blood vessels and injured tissues; usually occurs about a week after initial exposure; complement activation!

209
Q

Type IV Hypersensitivity

A

mediated by T cells; called “delayed reactions” since it takes a while (24-48 hours) for effective T cell recruitment to the site of inflammation

210
Q

ACID

A 
mnemonic for the types of hypersensitivity rxns
A - Allergy
C - Cytotoxic/antibody-mediated
I - Immune complex deposition
D - Delayed
211
Q

Autoimmune Hemolytic Anemia

A

Antibodies to own RBCs cause lysis of heme-containing erythrocytes, leading to anemia. (Type II hypersensitivity) Erythrocytes lost via:

  1. Phagocytosis from macrophages
  2. Lysis via complement MACs
212
Q

Hemolytic Disease of the Newborn (Erythroblastic Fetalis)

A

mother is Rh-negative (does not have Rh antigen on RBCs) but baby is Rh-positive (has Rh antigen thanks to dad); When baby’s blood gets into the mother’s circulation, she begins to produce IgG antibodies against Rh-positive erythrocytes; 1st baby is fine since he’s already born by the time mom’s antibodies are produced, but if there is 2nd pregnancy w/Rh-positive child, those antibodies can cross placenta and cause hemolysis

213
Q

RhoGAM

A

Pregnant Rh- mothers given prophylactic RhoGAM during and immediately following pregnancy to bind up all Rh+ erythrocytes and prevent mother’s sensitization

214
Q

Goodpasteure’s Syndrome

A

type II reaction involving linear deposition of IgG on glomerular basement membrane and lung; IgG binds a subunit of collagen type IV and can quickly lead to massive kidney and lung damage; treatment options include immunosuppressive steroids and plasmapheresis

215
Q

Graves Disease

A

example of non-cytotoxic type II rxn; Autoantibodies bind TSHr (thyroid stimulating hormone receptor) and mimic action of pituitary-produced TSH, constantly stimulating thyroid to produce hormones – hyperthyroidism

216
Q

autoantibodies

A

can either destroy self-antigens, or change the function of self-antigens

217
Q

2 examples of non-cytotoxic type II rxns

A

Graves Disease; Myasthenia Gravis

218
Q

Myasthenia Gravis

A

example of non-cytotoxic type II rxn; An autoantibody to skeletal muscle Ach receptors causes internalization and inactivation; fewer Ach receptors leads to muscle weakness and paralysis

219
Q

immune complexes

A

antibody-antigen complexes

220
Q

examples of Type III hypersensitivity reactions

A
  • systemic lupus erythematosus
  • polyarteritis nodosa
  • post-streptococcal glomerulonephritis
  • serum sickness
  • arthus reaction
221
Q

Precipitin Reaction

A

a solution containing antibody had antigen added to it until there was equivalence; centrifugation led to all antibody-bound antigens found in precipitant. If even more antigen was added until there was an excess, antigens were not completely coated by antibodies, but were rather bound by only a few antibodies and thus were in the supernatant after centrifugation because those complexes are so small. Small complexes are not cleared very well, and can force their way into glomeruli, blood vessel walls, and joint spaces, where they activate complement leading to basophil and neutrophil degranulation.

222
Q

antigen excess

A

there is way too much antigen and it’s usually very widespread, and the immune complexes that form are very small and tend to get deposited in all the wrong place. To clear it all out, we need a ton of antibodies, and those antibodies can overstimulate the complement and mast cell system to cause an overreaction

223
Q

Serum Sickness

A

Disease caused by injection of large doses of a protein antigen into the blood and characterized by the deposition of antigen-antibody (immune) complexes in blood vessel walls, especially in the kidneys and joints (Type III hypersensitivity). Immune complex deposition leads to complement fixation and leukocyte recruitment and subsequently to glomerulonephritis and arthritis. Was originally described as a disorder that occurred in patients receiving injections of serum containing antitoxin antibodies to prevent diphtheria.

224
Q

Arthus Reaction

A

Localized form of experimental immune complex–mediated vasculitis induced by injection of an antigen subcutaneously into a previously immunized animal or into an animal that has been given intravenous antibody specific for the antigen. Circulating antibodies bind to the injected antigen and form immune complexes that are deposited in the walls of small arteries at the injection site and give rise to a local cutaneous vasculitis with necrosis.

225
Q

Subacute Bacterial Endocarditis

A

Really slimy bacteria can adhere to the heart valves and become really tough to get rid of. The body mounts an antibody response but still can’t really clean up the heart valves effectively. Type III reaction, complement activation…eventually these patients need a massive dose of peniciilin to get back to normal function

226
Q

PPD test

A

determines whether you are sensitive to the tuberculosis-causing pathogen; Type IV hypersensitivity (T cell-mediated)

227
Q

Allergic Contact Dermatitis

A

type IV hypersensitivity; small molecules called haptens from an organism like poison ivy can infiltrate the skin and bind self-proteins. This modifies the molecular structure of the protein, and new antigenic determinant is recognized by immune system as foreign when presented in MHC complexes

228
Q

sensitization phase of Allergic Contact Dermatitis

A

first exposure – occurs as a normal immune response with no pathologic consequences, with APC migration to lymph node, T cell migration to skin, and then silence since the uptake and presentation is complete

229
Q

elicitation phase of Allergic Contact Dermatitis

A

subsequent exposure to antigen – Inflammatory mediators secreted by TH1 cells and keratinocytes recruit macrophages and PMNs to the site of exposure where the typical rash erupts and remains for a few days. (The element nickel is actually able to elicit this response without formation of a protein-hapten complex, solely via binding of TLR4, so stay away from cheap jewelry dealers.)

230
Q

Celiac Disease

A

immune overreaction to gluten; chronic, lifelong condition which, if untreated, can lead to irreversible intestinal villi damage; Acute episodes hallmarked by large inflammatory response, malabsorption, and diarrhea; avoidance of gluten-containing food products is enough to prevent symptoms

231
Q

celiac disease genetic expression

A

95% of patients with celiac disease have the HLA-DQ2 gene and phenotype (on MHC Class II), though not everyone who expresses HLA-DQ2 has celiac

232
Q

tissue transglutaminase (tTG)

A 
modifies gluten (and several other) peptides so they can bind MHC class II receptors after absorption through the gut epithelium; celiacs produce IgA antibodies against tTG
that cause an immune response anytime gluten is ingested
233
Q

most specific and sensitive way to diagnose celiac disease short of a biopsy?

A

Serum testing for anti-tTG antibodies

234
Q

Uticaria

A

hives – histamine release triggered by engagement of FcyRIII on mast cells

235
Q

wheat allergy vs celiac disease

A

wheat allergy = type I hypersensitivity

celiac = type IV hypersensitivity

236
Q

Silent celiac disease

A

Fulfill the definition of CD but patients have no symptoms

237
Q

Potential celiac disease

A

patients have specific antibodies characteristic of CD; May or may not have symptoms consistent with CD; Lack evidence of autoimmune insult to intestinal mucosa

238
Q

Latent celiac disease

A

Potential patients who have had a gluten-dependent enteropathy at some point in their life specific antibodies characteristic of CD; May or may not have symptoms consistent with CD; May or may not have auto-antibodies; These patients are rare as they would have had to be previously diagnosed as having CD but despite being on gluten, have a completely normal intestinal mucosa

239
Q

Congenital/primary immunodeficiency

A

caused by genetic defects that lead to blocks in the maturation or functions of different components of the immune system; usually onset in childhood

240
Q

acquired/secondary immunodeficiency

A

can result from a variety of causes; onset at any age

241
Q

immunodeficiency symptoms

A

infections, malignancies, autoimmune diseases, systemic symptoms

242
Q

opportunistic infections

A

only contract if you are immunocompromised

243
Q

Aspergillosis

A

common mold that people breathe in on a daily basis; immunocompromised people highly susceptible to health issues caused by this fungus

244
Q

B cell deficiency

A

absent/reduced follicles and germinal centers in lymphoid organs; reduced serum IgG; pyogenic and enteric bacterial and viral infections

245
Q

T cell deficiency

A

reduced T cell zones in lymphoid organs; reduced DTH rxns to common antigens; defective T cell proliferative responses to mitogens in vitro; viral and other intracellular microbial infections, plus virus-associated malignancies

246
Q

innate immune deficiency

A

symptoms variable depending on defective component; pyogenic bacterial and viral infections

247
Q

immunodeficiency diseases

A

Disorders caused by defective immunity

248
Q

examples of acquired/secondary immunodeficiency

A

HIV/AIDS

249
Q

examples of congenital/primary immunodeficiency

A

SCID

250
Q

SCID

A

Disorders manifesting as defects in both the B cell and T cell arms of the adaptive immune system

251
Q

X-linked SCID

A

deficiencies: markedly decreased T cells, normal/increased B cells, reduced serum Ig
mechanism: cytokine receptor common gamma chain gene mutations, defective T cell maturation due to lack of IL-7

252
Q

Autosomal recessive SCID due to ADA, PNP deficiency

A

deficiencies: progressive decrease in T (mainly) & B cells, reduced serum Ig (ADA); normal B cells & serum Ig (PNP)
mechanism: accumulation of toxic metabolites in lymphocytes

253
Q

Autosomal recessive SCID due to other causes

A

deficiencies: decreased T & B cells, reduced serum Ig
mechanism: defective maturation of T & B cells; may be mutations in RAG genes and other genes involved in VDJ recomb/IL-7R signaling

254
Q

X-linked agammaglobulinemia

A

B cell immunodeficiency

deficiencies: decrease in all serum Ig isotypes; reduced B cells; often meningitis
mechanism: block in maturation beyond pro-B cells due to mutation in Bruton tyrosine kinase (BTK)

255
Q

Bruton tyrosine kinase

A

mutation causes X-linked agammaglobulinemia (B cell immunodeficiency)

256
Q

Ig heavy chain deletions

A

B cell immunodeficiency

deficiencies: IgG1, IgG2, or IgG4 absent, sometimes IgA or IgE absent
mechanism: chromosomal deletion at 14q32

257
Q

DiGeorge Syndrome

A

T cell immunodeficiency

deficiencies: decreased T cells, normal B cells, normal/decreased serum Ig
mechanism: anomalous development of 3rd & 4th branchial pouches leading to thymic hypoplasia; 22q11.2 deletion

258
Q

cytokine receptor common gamma chain (Υc) gene

A

mutations cause more than 99% of cases of X-linked SCID

259
Q

IL-7

A

defects affect T cell maturation

260
Q

adenosine deaminase (ADA)

A

mutations cause about half of the cases of autosomal SCID – accumulation of toxic metabolites in proliferating cells causes greater deficiency in T cells than B cells

261
Q

purine nucleotide phosphorylase (PNP)

A

causes autosomal SCID – accumulation of toxic metabolites in proliferating cells causes greater deficiency in T cells than B cells

262
Q

RAG1 / RAG2 genes

A

encode the VDJ recombinase that is required for Ig and T cell receptor gene recombination and lymphocyte maturation; mutations cause rare cases of autosomal SCID

263
Q

most common clinical syndrome caused by a block in B cell maturation?

A

X-linked / Bruton’s agammaglobulinemia

264
Q

most widely used treatment for SCID?

A

hematopoietic stem cell transplantation

265
Q

treatment for X-linked agammaglobulinemia?

A

Ig replacement therapy

266
Q

X-linked hyper-IgM syndrome

A

defects in helper T cell-dependent B cell and macrophage activation caused by mutations in CD40 ligand

267
Q

mutations in CD40 ligand

A

cause X-linked hyper-IgM syndrome (defects in helper T cell-dependent B cell and macrophage activation)

268
Q

common variable immunodeficiency (CVID)

A

mutations in receptor for B cell growth factors, costimulators, cause reduced/no production of select Ig isotypes; can cause recurrent infections, autoimmune disease, and lymphomas

269
Q

Bare Lymphocyte Syndrome

A

mutations in genes encoding TFs for MHC Class II expression cause lack of MHC II expression and impaired CD4+ T cell activation, leading to defective cell-mediated immunity and T-cell dependent humoral immunity

270
Q

Defects in T cell receptor complex expression/signaling

A

mutations/deletions in genes encoding CD3 proteins or ZAP-70; rare; cause decreased T cells or abnormal ratios of CD4+/CD8+ subsets, leading to decreased cell-mediated immunity

271
Q

Defects in Th1 responses

A

mutations in genes encoding IL-2 receptors or IFN-gamma; rare; cause decreased T cell-mediated macrophage activation and susceptibility to intracellular microbial infection

272
Q

Defects in Th17 responses

A

mutations in genes encoding STAT3, IL-17, IL-17R; rare; cause decreased T cell-mediated inflammatory responses and susceptibility to infections with pyogenic bacteria and mucocutaneous candidiasis

273
Q

X-linked lymphoproliferative syndrome

A

mutations in SAP cause uncontrolled EBV-induced B cell proliferation, uncontrolled macrophage and CTL activation, defective NK cell and CTL function

274
Q

Pneumocystis jiroveci

A

a fungus that survives within phagocytes in the absence of T cell help; boys with X-linked hyper-IgM syndrome are susceptible

275
Q

Chronic granulomatous disease

A

mutations in genes encoding subunits of phagocyte oxidase cause inability to kill phagocytosed microbes; immune system calls in more macrophages and activates T cells, which recruit more phagocytes – leads to collections of phagocytes around infections (granulomas)

276
Q

Leukocyte adhesion deficiency

A

caused by mutations in genes encoding integrins, molecules required for expression of ligands for selectins, or signaling molecules activated by chemokine receptors required to activate integrins; blood leukocytes do not bind firmly to vascular endothelium and are not recruited normally to sites of infection

277
Q

Complement C3 Deficiency

A

mutations in C3 gene cause defects in complement activation; usually fatal

278
Q

Complement C2/C4 Deficiency

A

mutations in C2/C4 genes cause deficient activation of classical pathway

279
Q

Chediak-Higashi Syndrome

A

mutation in gene encoding lysosomal trafficking regulatory protein causes defective lysosomal function in neutrophils/macrophages/DCs and defective granule function in NK cells

280
Q

Herpes Simplex 1 encephalitis

A

mutations in gene encoding TLR3 cause defective antiviral immunity in CNS

281
Q

recurrent bacterial pneumonia

A

mutations in gene encoding MyD88 cause defective innate immune responses to pyogenic bacteria

282
Q

Wiskott-Aldrich syndrome

A

X-linked disease characterized by eczema, thrombocytopenia (reduced platelets), and immunodeficiency manifested as susceptibility to bacterial infections; defective gene encodes a cytosolic protein involved in signaling cascades and regulation of the actin cytoskeleton

283
Q

Ataxia-telangiectasia

A

characterized by gait abnormalities (ataxia), vascular malformations (telangiectasia), and immunodeficiency; caused by mutations in a gene whose product is involved in DNA repair; defects in this protein lead to abnormal DNA repair (e.g., during recombination of antigen receptor gene segments), resulting in defective lymphocyte maturation.

284
Q

HIV attacks what?

A

CD4+ cells

285
Q

irradiation and chemotherapy treatments for cancer cause what problem?

A

decreased bone marrow precursors for all leukocytes

286
Q

immunosuppression for graft rejection and inflammatory diseases causes what problem?

A

depletion or functional impairment of lymphocytes

287
Q

involvement of bone marrow by cancers causes what problem?

A

reduced site of leukocyte development

288
Q

protein-calorie malnutrition causes what problem?

A

metabolic derangements that inhibit lymphocyte maturation and function

289
Q

spleen removal causes what problem?

A

decreased phagocytosis of microbes

290
Q

AIDS

A

caused by HIV infection; defined by a CD4+ count of less than 200 cells/mm3 or an AIDS-defining illness

291
Q

HIV

A

retrovirus that infects and destroys cells of the immune system, mainly CD4+ T lymphocytes; infects via major envelope glycoprotein (gp120)

292
Q

HIV life cycle

A
  • infection of cells
  • production of viral DNA
  • integration of viral DNA into host genome
  • production of viral particles
293
Q

gp120

A

major envelope glycoprotein of HIV; binds to CD4 and particular chemokine receptors – mainly CXCR4 on T cells and CCR5 on macrophages

294
Q

provirus

A

viral DNA integrated into host DNA

295
Q

HIV virion binds to what?

A

CD4 and chemokine receptors on T cells – gp120 binds to CD4, then after conformational change, binds CCR5/CXCR4

296
Q

Most cases of AIDS are caused by?

A

HIV-1

297
Q

During the course of HIV infection, the major source of infectious viral particles is?

A

activated CD4+ cells

298
Q

what cells serve as reservoirs of infection in HIV?

A

dendritic cells and macrophages

299
Q

depletion of CD4+ T cells after HIV infection is caused by?

A

cytopathic effect of the virus, resulting from production of viral particles in infected cells, as well as death of uninfected cells

300
Q

clinical features of HIV infection

A
  • early mild acute illness which subsides within a few days
  • clinical latency w/progressive loss of CD4+ T cells in lymph tissues and destruction of architecture of lymph tissues
  • blood CD4+ count begins to decline
  • AIDS when CD4+ count <200 cells/mm^3
301
Q

clinicopathologic manifestations of full-blown AIDS are primarily the result of?

A

increased susceptibility to infections and some cancers, as a consequence of immune deficiency

302
Q

Pneumocystis jiroveci

A

aka PCP pneumonia; AIDS patients particularly susceptible, so often take prophylactic bactrim

303
Q

bactrim

A

prophylactic against PCP pneumonia; recommended daily for AIDS patients

304
Q

how does AIDS affect CD8+ cells?

A

Patients with AIDS show defective CTL responses to viruses, even though HIV does not infect CD8+ T cells, probably because CD4+ helper T cells are required for full CD8+ CTL responses against many viral antigens

305
Q

two most common types of cancers caused by oncogenic viruses in AIDS patients?

A

B cell lymphomas, caused by the Epstein-Barr virus, and a tumor of small blood vessels called Kaposi’s sarcoma, caused by a herpesvirus

306
Q

Epstein-Barr virus

A

causes B cell lymphomas

307
Q

Kaposi’s sarcoma

A

tumor of small blood vessels caused by a herpesvirus

308
Q

immune responses to HIV

A

Infected patients produce antibodies and CTLs against viral antigens, and the responses help to limit the early, acute HIV syndrome, but these immune responses usually do not prevent progression of the disease

309
Q

why are CTLs often ineffective in killing HIV-infected cells?

A

the virus inhibits the expression of class I MHC molecules by the infected cells

310
Q

elite controllers

A

A small fraction of patients control HIV infection without therapy

311
Q

HLA-B57 and HLA-B27

A

presence of these molecules seems to be protective against HIV, perhaps because they are particularly efficient at presenting HIV peptides to CD8+ T cells.

312
Q

current treatment for AIDS is aimed at?

A

controlling replication of HIV and the infectious complications of the disease

313
Q

highly active antiretroviral therapy (HAART) / combination antiretroviral therapy (ART)

A

Combinations of drugs that block the activity of the HIV viral reverse transcriptase, protease, and integrase enzymes administered early in the course of the infection

314
Q

wasting syndrome

A

significant loss of body mass, caused by altered metabolism and reduced caloric intake

315
Q

AIDS dementia

A

likely caused by infection of macrophages (microglial cells) in the brain

316
Q

Fc portions of Ig molecules

A

made up of the heavy-chain constant regions; contain the binding sites for Fc receptors on phagocytes and for complement proteins

317
Q

Fc regions

A

antibodies use these to activate diverse effector mechanisms that eliminate microbes and toxins

318
Q

Fab regions

A

antibodies uses these to bind to and block the harmful effects of microbes and toxins

319
Q

IgG

A
  • neutralization of microbes & toxins
  • opsonization of antigens
  • activation of classical complement
  • ADCC mediated by NK cells
  • neonatal immunity
  • feedback inhibition of B cell activation
320
Q

IgM

A

activation of classical complement

321
Q

J chain important for which Ig isotypes?

A

IgA, IgM

JAM!

322
Q

which Ig isotypes activate classical complement?

A

IgG, IgM

GM makes classic cars

323
Q

IgA

A
  • mucosal immunity
  • secretion into lumens of GI, respiratory tracts
  • neutralization of microbes, toxins
324
Q

IgE

A
  • mast cell degranulation (allergic rxn)

- defense against helminths

325
Q

22q11.2 deletion

A

causes DiGeorge Syndrome (T cell deficiency)

326
Q

DiGeorge Syndrome classic triad of symptoms

A
  1. cardiac anomalies
  2. hypoplastic thymus w/immunodeficiency
  3. hypoplastic parathyroid w/hypocalcemia
327
Q

Δ32 CCR5 mutations

A

protective against HIV since this is how HIV virions bind macrophage CD4 receptors; also increase susceptibility to plague and west nile virus

328
Q

which 3 drugs are HIV patients usually on?

A
  1. reverse transcriptase inhibitor
  2. integrase inhibitor
  3. protease inhibitor
329
Q

4 steps of HIV clinical course

A
  1. Primary infection
  2. acute infection
  3. clinical latency
  4. AIDS
330
Q

B cell deficiencies generally cause what?

A
  • Recurrent pyogenic bacterial infection (particularly encapsulated bacteria)
  • Enteric bacterial and viral infections
331
Q

T cell deficiencies generally cause what?

A
  • Viral infections
  • Opportunistic infections (esp. intracellular microbial infections)
  • Virus-associated malignancies
332
Q

Examples of Defects in Lymphocyte Maturation

A
  • Severe combined immunodeficiency (SCID)
  • X-linked (Bruton’s) agammaglobulinemia
  • DiGeorge Syndrome
333
Q

Examples of Defects in Lymphocyte Activation or Function

A
  • Common Variable Immunodeficiency (CVID)
  • X-linked hyper-IgM syndrome
  • Bare lymphocyte syndrome
334
Q

Examples of Defects in Innate Immunity

A
  • Chronic Granulomatous Disease (CGD)
  • Leukocyte Adhesion Deficiency
  • Complement deficiencies
  • Chédiak-Higashi Syndrome
335
Q

how to diagnose SCID?

A

low T cells (absolute lymphocyte count OR maternal T cells – CD45RO – in circulation)

336
Q

how to diagnose CVID?

A
  • Markedly reduced serum IgG + low IgM/IgA

- Poor or absent response to vaccines

337
Q

how to diagnose X-linked hyper-IgM Syndrome?

A
  • defective class-switch recombination
  • normal/increased IgM
  • deficient IgG, IgA, IgE
338
Q

how to diagnose CGD?

A

Nitroblue tetrazolium test

339
Q

how to diagnose C3 deficiency?

A

CH50 test

340
Q

live attenuated vaccine

A

a living microbe that has been weakened in the laboratory so it does not cause disease; very immunogenic & long-lasting but contraindicated in immunocompromised pts and could mutate into more virulent strain

341
Q

most immunogenic type of vaccine?

A

live attenuated

342
Q

immunogenic

A

stimulates immune response

343
Q

types of live attenuated vaccines

A 
Oral polio
MMR
varicella
oral typhoid
smallpox
yellow fever
BCG
zoster
344
Q

what type of cell is important for immune response to live attenuated vaccines?

A

CD8+ (viral/intracellular pathogen defense)

345
Q

inactivated vaccine

A

microbes that have been killed by chemicals, heat, or radiation; induce T cell-dependent B cell response but less immunogenic than live attenuated and more side effects

346
Q

types of inactivated vaccines

A

Inactivated polio
hepatitis A
rabies

347
Q

toxoid vaccines

A

Made from formalin-inactivated toxins

348
Q

types of toxoid vaccines

A

tetanus

diptheria

349
Q

Subunit Vaccines

A

Contain only antigens which best stimulate the immune system, extracted from whole organisms or produced through recombinant DNA technology; induce T cell-dependent B cell response but less immunogenic than live attenuated and inactivated vaccines

350
Q

types of whole organism subunit vaccines

A 
Acellular pertussis
influenza
pneumococcus
meningococcus
IM typhoid
351
Q

types of recombinant subunit vaccines

A

HBV

HPV

352
Q

Conjugate Vaccines

A

Linking polysaccharide antigens to proteins to better stimulate the immune system, and allow the antigens to be recognized by T cells

353
Q

Types of Conjugate Vaccines

A

HiB
pneumococcus
meningococcus

354
Q

Polysaccharide Vaccines

A

type of subunit vaccine that do not induce long-lasting immunity because T cells only recognize peptide-MHC complexes, and in order for a B cell to develop into a memory B cell it must have the help of a CD4+ T cell during the germinal center reaction; generates T-independent B cell response w/lower affinity antibodies; no germinal center reaction; no memory B cells; no “booster” effect w/2nd vaccination

355
Q

which type of vaccine is not effective in children under age 2, gives the least robust response, and does not prevent colonization?

A

polysaccharide vaccines

356
Q

vaccine trade-offs

A

immunogenicity of vaccine vs potential increased risk to patient by using that type of vaccine

357
Q

recent resurgence of pertussis due to?

A

substitution of the whole cell with acellular pertussis in the 1990s (less immunogenic, but fewer side effects)

358
Q

Adjuvants

A

substances added to a vaccine to increase immune system stimulation but not cause too much damage; allows use of less of actual antigen in vaccine to get same immune response

359
Q

types of adjuvants

A
  • Aluminum salts (most common)
  • Oil in water
  • TLR agonists
  • Liposomes
360
Q

routes of vaccine administration

A
  • intramuscular
  • subcutaneous
  • intradermal
  • oral
  • intranasal
361
Q

which type of vaccine administration best with adjuvants?

A

intramuscular (DTaP)

362
Q

which type of vaccine administration best for live attenuated?

A

subcutaneous (MMR)

363
Q

which type of vaccine administration best for dose-sparing?

A

intradermal - more dendritic cells just under skin (BCG)

364
Q

which type of vaccine administration best for inducing mucosal immunity?

A

oral (polio) or intranasal (influenza)

365
Q

3 main considerations for timing of vaccination

A

1) Age at administration
2) Spacing between doses
3) Co-administration of multiple vaccines

366
Q

The age at which a vaccine is administered depends on?

A

1) Presence of maternal antibodies (will remain as long as breastfeeding)
2) maturity of immune system
3) risk of exposure to disease

367
Q

spacing between doses of vaccine?

A
  • 3 week minimum btwn primary doses
  • 4 month minimum btwn primary and boosters
  • NO max interval in terms of immune response
368
Q

maximum interval between vaccine doses?

A

does not exist – artificial “deadline” in the interest of getting patients protected as soon as possible

369
Q

Co-administration of Multiple Vaccines

A

Live vaccines should either be given simultaneously or greater than or equal to one month apart b/c they tend to elicit a large-scale systemic response; no interference w/inactivated vaccines

370
Q

Herd Immunity

A

the reduction of diseases in an unimmunized segment of the population in which a large portion of the population has been immunized

371
Q

R0

A

basic reproduction number – number of secondary cases generated by an infectious individual in a fully susceptible population; takes into account how crowded an area is.

372
Q

which is better: a low or high R0?

A

low - this means there are fewer 2ndary cases generated by an infectious individual

373
Q

(R0 – 1)/R0

A

threshold of proportion of immune individuals needed in a population. Over this number, the incidence of the infection will decrease. If the immunized proportion is equal to this number, the incidence of disease will remain the same.

374
Q

types of pathogens that pose major challenges for vaccine development

A
  • pathogens for which there is no natural immunity (HIV, CMV, HSV)
  • pathogens that mutate rapidly (influenza, HIV)
  • pathogens w/multiple serotypes (rhinovirus, group A strep, Dengue fever)
375
Q

the only disease that has been fully eradicated through vaccination?

A

smallpox

376
Q

1st Known Vaccination

A

1774 - cowpox experiment

377
Q

vaccines not yet used commercially

A

DNA and Recombinant Vector Vaccines

378
Q

TH1

A

Phagocytosis and complement!

  • produce IFN-γ, IL-12
  • TFs: STAT1, STAT4, T-bet
  • activate phagocytes to eliminate ingested microbes
  • stimulate production of opsonizing and complement-binding antibodies
379
Q

TH2

A

Allergy and parasite defense!

  • produce IL-4, IL-5, IL-13
  • TFs: STAT3, GATA3
  • stimulate IgE production
  • activate M2 macrophages
  • activate eosinophils, which function mainly in defense against helminths
380
Q

TH17

A

Inflammation and infection!

  • produce TGF-beta, IL-17, IL-22
  • TFs: RORyT
  • play a role in defense against extracellular bacterial and fungal infections
  • implicated in several inflammatory diseases
381
Q

CD8+ effector molecules

A
  • Perforin & Granzymes
  • FasL-Fas
  • TNF-alpha & IFN-gamma
  • NF-κB/Stat-1
382
Q

IL-2

A

major growth factor for T cell proliferation and differentiation; also NK cell proliferation and activation; deficiency can cause autoimmunity

383
Q

IFN-gamma

A
  • activation of M1 macrophages
  • TH1 differentiation
  • B cells – isotype switching to opsonizing and complement-fixing IgG subclasses
  • increased expression of MHC Class I & II
  • increased antigen processing & presentation to T cells
384
Q

TNF-alpha

A
  • activation of endothelial cells (inflammation)

- activation of neutrophils

385
Q

IL-3

A

induced maturation of all hematopoietic lineages

386
Q

IL-4

A

B cells - isotype switching to IgE
TH2 differentiation
M2 macrophage activation

387
Q

IL-5

A

activation and increased generation of eosinophils (TH2)

B cells - IgA production

388
Q

IL-6

A

B cells - proliferation of antibody-producing cells

389
Q

IL-7

A

proliferation of early T and B cell progenitors; survival of naive and memory T cells

390
Q

IL-9

A

produced by CD4+ cells; promotes survival & activation of mast cells, B cells, T cells, and tissue cells

391
Q

IL-12

A
  • TH1 differentiation

- induces IFN-gamma synthesis, increased cytotoxic activity of NK cells and CD8+ cells

392
Q

IL-13

A

produced by TH2 cells

  • B cells - isotype switching to IgE
  • increased mucus production
  • increased collagen synthesis
  • M2 macrophage activation
393
Q

IL-17

A

produced by TH17 cells

  • increased chemokine production by endothelial cells and macrophages
  • increased GM-CSF production
394
Q

Molecular mimicry

A

the postulated mechanism whereby immune responses to a microbe containing antigens that cross-react with self antigens may trigger an autoimmune response. This autoimmune response may then persist, even in the absence of the inciting microbe

395
Q

T cell threshold of activation

A

In general, the TCR binds to peptide-MHC complexes with lower affinity than antigen-antibody interactions. This relatively low-affinity interaction occurs briefly; thus, a T cell may need multiple engagements with the antigen- presenting cell (APC) before a threshold of activation occurs. If this threshold is not reached, the T cell may become anergic

396
Q

IL-21

A

produced by TH17 cells

  • activation, proliferation, differentiation of B cells
  • increased generation of TH17 cells
397
Q

IL-10

A

produced by M2 macrophages, regulatory T cells

- inhibition of IL-12, costimulators, and MHC Class II (anti-inflammatory)

398
Q

IL-22

A

produced by TH17 cells

  • production of defensins
  • increased epithelial barrier function
  • survival of hepatocytes
399
Q

IL-1

A

produced by macrophages, DCs, etc

- activation of endothelial cells (inflammation)

400
Q

TGF-beta

A

produced by regulatory T cells

  • inhibition of T cell proliferation and effector functions
  • differentiation of TH17 and Treg
  • inhibition of B cell proliferation
  • IgA production
  • inhibition of macrophage activation
401
Q

examples of Type II hypersensitivity reactions

A
  • Autoimmune Hemolytic Anemia
  • Hemolytic Disease of the Newborn (Erythroblastic Fetalis)
  • Goodpasteure’s Syndrome
  • Graves Disease
  • Myasthenia Gravis
402
Q

adhesion molecules in naive T cells

A

L-selectin
LFA-1
CCR7

403
Q

adhesion molecules in activated T cells

A

E- and P-selectin Ligand
LFA-1 or VLA-4
CXCR3

404
Q

CD28

A

a feature of naïve T cells which provides costimulation (with B7) during activation by dendritic cell

405
Q

CD40L

A

upregulated after activation of a CD4+ T cell; provides costimulation for interactions between the helper T cell and the cells it is helping (B cells, macrophages)

406
Q

which part of antibody determines function?

A

constant region of heavy chain

407
Q

immature B cells express?

A

IgM

408
Q

mature B cells express?

A

IgM and IgD

409
Q

what kinds of recombination occur in B cell heavy and light chains?

A
  • heavy: VDJ

- light: VJ

410
Q

germinal center reaction

A

B cell activation and proliferation due to interaction with

antigen and helper T cell

411
Q

somatic hypermutation

A

germinal center reaction generates high-affinity

antibodies via changes in complementarity-determining region

412
Q

affinity maturation

A

B cells produce antibodies with increased affinity for antigen during the course of an immune response; depends on somatic mutation of V genes

413
Q

2 ways to activate B cell

A
  1. T cell-dependent

2. T cell-independent

414
Q

T cell-dependent B cell activation

A

activated CD4+ cell recognizes antigen on B cell and uses CD40L to bind to CD40 on B cell (2 signals)

415
Q

T cell-independent B cell activation

A

B cell is exposed to antigen that also binds complement receptor CR2; this activates the B cell without T cell participation; This method is much faster than T cell-dependent activation but the B cell cannot do as much (no isotype switching); B cell recognizes antigen and activated complement bound to antigen (2 signals)

416
Q

what does a B cell need to be able to switch Ig isotypes?

A

T cell activation!

417
Q

Isotype switching

A

permanently alters the germline DNA to attach a new C region to the end of the Ig gene

418
Q

AID enzyme

A

induces Somatic Hypermutation, Gene Conversion and Isotype Switching in activated B cells

419
Q

APE1

A

the DNA repair enzyme that allows a new C region to be joined to the variable region of the Ig gene: class switching of isotypes

420
Q

FcyRI

A

activation of phagocytes

421
Q

FcyRIIA

A

phagocytosis

422
Q

FcyRIIIA

A

ADCC (NK Cells)

423
Q

FceRI

A

activation of mast cells, eosinophils

424
Q

C50 test

A

determines if a patient has high or low complement activity

425
Q

complement opsonizers

A

C3b, C4b

426
Q

complement inflammatory stimulators

A

C3a, C5a

427
Q

IFN-alpha

A
  • activation of NK cells
  • enhanced expression of MHC Class I molecules
  • accelerated degradation of viral RNA

M1 - Immuno (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions