Brainscape's Knowledge GenomeTM

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


See full index

FMS Week 9 > Week 9 review > Flashcards

Week 9 review Flashcards

1
Q

Central T cell tolerance

A

Negative selection of high affinity T cells in the thymus

expression of tissue specific proteins in the thymus (via AIRE) so that they participate in negative selection of T cells

positive selection in the thymus serts an affinity threshold

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

Peripheral tolerance of T cells

A

suppression of responses by regulatory T cells (which compete for growth factors, secrete inhibitory cytokines, and directly inhibit T cells)

unresponsiveness of T cells without co-stimulatory signals

exclusion of lymhocytes from certain peripheral tissues (brain, eyes, testes)

Downregulation of responses (CTLA-4, PD-1, Fas/FasL killing)

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

No autoreactive TH cells means…

A

no autoantibodies

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

If B cell sees self antigen but it does not get T help,

A

it will not get activated

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

Overview of B cell tolderance

negative selection in the bone marrow

if B cell sees self antigen but doesnt get T help it will not be activated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which of the following is a PERIPHERAL tolderance mechanism used by both B and T cells?

Negative selection

regulatory T cells

receptor editing

antigen sequestration

allelic exclusion

A

ANTIGEN SEQUESTRAITON

negative selection-central tolerance mechanism

regulatory T cells- can down regulate T helper

receptor editing- B cells in the bone marrow. CENTRAL.

allelic exclusion- doesnt mean anything

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

Which one of the following statements concearning autoimmune disease is true?

autoimmunity manifests as organ-specific, not systemic, disease

infectious organisms are frequently present in autoimmine lesions

effector mechanisms in autoimmunity include curculating autoantibodies, immune complexes, and autoreactive T lymphocytes

among the genes associated with autoimmunity, associations are particularly prevalent with class I MHC genes

many autoimmune diseqases show higher incidence in males than females

A

effector mechanisms in autoimmunity include curculating autoantibodies, immune complexes, and autoreactive T lymphocytes

autoimmunity is more associated with class II MHC genes

autoimmunity usually higher in males than females

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

Type I hypersensativity

A

AKA immediate hypersensativity

TH2 cells, IgE, mast cells, eosinophils

mechanism of injury
mast cell derived mediators (vasoactive amines, lipid mediators, cytokines)

cytokine mediated inflammation (eosinophils, neutrophils)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Type II hypersensativity

A

antibody mediated

IgM, IgG antibodies against cell surface or ECM antigens

Complement and Fc receptor mediated recruitment and activation of leukocytes (neutrophils, macrophages)

opsonization and phagocytosis of cells

abnormalities in cellular function ed hormone receptor signaling

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

Type III hypersensativity

A

immune complex mediated

Immune complexes of circulating antigens and IgM or IgG antibodies deposited in basement membrane

complement and Fc receptor mediated recruitment and activation of leukocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

type IV hypersensativity

A

T cell mediated diseases

CD4+ T cells, (delayed type hypersensativity)

CD8+ CTLs (T cell mediated cytolysis)

macrophage activation, cytokine mediated inflammation

direct target cell lysis, cytokine mediated inflammation

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

DTH and PPD antigens

A

type IV hypersensativity

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

Autoimmune hemolytic anemia

A

Type II hypersensativity

Target antigen: erythrocyte membrane protein

mechanism of disease: opsonization and phagocytosis of RBC

clinicopathologic manifestations: hemolysis, anemia

LYSIS OF CELL

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

Autoimmune (idiopathic) thrombocytopnic purpura

A

Type II hypersensativity

Target antigen: PLATELET MEMBRANE

mechanism of disease: OPSONIZATION AND PHAGOCYTOSIS OF PLATELETS

clinicopathologic manifestations: BLEEDING

lysis of cells!

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

Pemphigus vulgaris

A

Type II hypersensativity

Target antigen: proteins in intracellular junctions of epidemal cells (epidermal cadherins)

mechanism of disease: antibody mediated activation of proteases, disruption of intracellular adhesions

clinicopathologic manifestations: skin vessicles (bullae)

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

Goodpastures syndrome

A

Type II hypersensativity

Target antigen: noncollagenous protein in basement membranes od kidney glomeruli and lung alveoli

mechanism of disease: complement and Fc receptor mediated inflammation

clinicopathologic manifestations: nephritis, lung hemorrhages

inflammation

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

Acute rheumatic fever

A

Type II hypersensativity

Target antigen: streptococcal cell wall antigen; antibody cross-reacts with myocardial antigen

mechanism of disease: inflammation, macrophage activation

clinicopathologic manifestations : myocarditis, arthritis

MOLECULAR MIMICRY

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

Myesthenia gravis

A

Type II hypersensativity

Target antigen: Ach receptor

mechanism of disease: antibody inhibits acetylcholine binding. Down modulates receptors (ab blocks binding site)

clinicopathologic manifestations: muscle weakness, paralysis

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

Graves disease (hyperthyroidism)

A

Type II hypersensativity

Target antigen: thyroid stimulating hormone receptor (TSH)

mechanism of disease: antibody mediated stimulation of TSH receptors

clinicopathologic manifestations: hyperthyroidism

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

Pernicious anemia

A

Type II hypersensativity

Target antigen: intrinsic factor of gastric parietal cells

mechanism of disease: neutralization of intrinsic factor. decreased absorption of vitamin B12

clinicopathologic manifestations: abnormal erythopoesis, anemia

AB MEDIATED INHIBITION OF FUNCTION

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Systemic lupus erythematosus

A

Type III hypersensativity

Antibody specificity: DNA, nucleoproteins, others

Clinical manifestations: nephritis, arthritis, vasculitis, renal failure

Antibuclear Abs (ANA)

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

Serum sickness (clinical and experimental)

A

Antibody specificity: various protein antigens

Clinical manifestations: systemic vasculitis, nephritis, arthritis

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

SLE

A

displays more than one type of hypersensativity reaction

immune complexes (type III) mediating vasculitis, serositis,glomerulonephritis, arthritis, rash and oral ulcers, pericardial and pleural effusions,

Coomb’s positive hemolytic anemia (type II)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Type 1 (ID) DM

A

Type IV hypersensativity reaction

Specificity of pathogenic T cells: pancreatic islet antigens

Genetic associations: insulin, PTPN22

Clinicopathologic manifestations: impaired glucose metabolism, vascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Rheumatoid arthritis

A

Type IV hypersensativity reaction

Specificity of pathogenic T cells: unknown antigens in joint

Genetic associations: PTPN22

Clinicopathologic manifestations: inflammation of synovium and erosion of cartilage and bone in joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

multiple sclerosis

A

Type IV hypersensativity reaction

Specificity of pathogenic T cells: myelin proteins

Genetic associations: CD25

Clinicopathologic manifestations: demyelination of neurons in the CNS, sensory and motor dysfunction

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

Contact sensativity (eg poison ivy reaction)

A

Type IV hypersensativity reaction

Specificity of pathogenic T cells: modified skin proteins

Clinicopathologic manifestations: DTH reaction in the skin, rash

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Superantigen mediated diseases (toxic shock syndrome)

A

Type IV hypersensativity reaction

Specificity of pathogenic T cells: polyclonal (microbial superantigens activate many T cells of different specificites

Clinicopathologic manifestations: fever, shock related to systemic inflammatory cytokine release

Superantigen mediated- pathogen (microbial superantigen) activated T cells

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

Hypersensativity and allergy

A

Components: TH2, IgE, mast cells (mucosal/connective tissue), basophils (blood), and eosinophils (blood)

Mechanism of injury: mast cell derived mediators such as vasoactive amines such as histamine, lipid mediators, and cytokines ( IL4, IL5, IL13)

Processes: vascular dilation (vasoactive amines and prostaglandins)

Tissue damage (proteases)

Smooth muscle contraction ( vasoactive amines and leukotrienes)

inflammation and recruitment of leukocytes (cytokines)

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

Steps in allergy

A

first exposure to allergen

antigen activation of TH2 cells and stimulation of IgE class switching in B cells

Production of IgE

Binding of IgE to FCeRI on mast cells

Repeate exposure to allergen

activation of mast cells and release of mediators

Vasoactive amines, lipid mediators: immediate hypersensativity reaction (minutes after repeat exposure to allergen)

Cytokines: late phase reaction (6-24 hours after repeat exposure to allergen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

In an experiment, antigen is used to induce immediate (type I) hypersensativity response. Cytokines are secreated that are observed to stimulate IgE production by B cells, promote mast cell growth, and recruit and activate eosinophils in this response. Which of the following cells is the most likely to be the source of these cytokines?

TH2 cells

TH1 cells

Mast cells

Eosinophils

Dendritic cells

A

TH2 cells

32
Q

A woman who is allergic to cats visits a neighbor who has several cats. During the visit she inhales cat dander, and within minutes, she develops nasal congestion and abundant nasal secretions. Which of the following substances is most likely to produce these findings?

Complement C5a

Histamine

IL-1

Phospholipase C

Numor Necrosis Factor (TNF)

A

HISTAMINE

33
Q

Mediators stored in preformed cytoplasmic granules

A

Immediate response

histamine

enxymes: tryptase, chymase, carboxypeptidase, cathepsun G

TNFalpha

34
Q

Histamine

A

increases vasc perm, stim smooth muscle cell contraction, toxic to parasites

35
Q

Enzymes: tryptase, chymase, carboxypeptisase, cathepsin G

A

tissue damage/ remodeling; degrades microbial structures

36
Q

TNF alpha

A

promotes inflammation, activated endothelium

immediate response

37
Q

Major lipid mediators produces on activation

A

late phase response

prostaglandin D2

Leukotriene C4, D4, E4

Platelet activating factor

38
Q

Prostaglandin D2

A

vasodilation, bronchoconstriction, neutrophil chemotaxis

39
Q

Leukotriene C4, D4, E4

A

prolonged bronchoconstriction

mucus secretion

increased vasc perm

40
Q

platelet activating factor

A

late phase response

lipid mediator

chemotaxis and activation of leukocytes (eosinophils and neutrophils) and platelets, bronchoconstriction, increased vasc perm

41
Q

Cytokines/ chemokines produced on activation (by mast cells after cross linking)

A

IL3

TNF alpha

IL4

IL13

IL5

CCL3

42
Q

IL3

A

promotes mast cell proliferation

43
Q

TNFa

A

promotes inflammation

44
Q

IL4 IL13

A

promotes Th2 differentiation, mucus production

45
Q

IL5

A

promotes eosinophil production and activation

46
Q

CCL3

A

chemotactic for monocytes, macrophages, neutrophils

47
Q

Type I hypersensativity reaction of skin

A

wheal and flare (immediate)

Swelling (late phase)

48
Q

Type I hypersensativity reaction of resp tract

A

rhinitis

polyps

asthma

eosinophils

49
Q

Type I hypersensativity reaction of digestive tract

A

diarrhea, cramps, vomiting

50
Q

Type I hypersensativity reaction systemimc

A

anaphylactic shock

edema

circulatory collapse

tracheal occlusion

51
Q

Hyperacute rejection

A

minutes to hours

rapid and mediated by circulating antibodies which activate coplement, leading to endothelial damage and thrombosis

Already circulating Abs against something in graft

52
Q

Accelerated rejection

A

days

reactivation of sensitized T cells

53
Q

Acute rejection

A

days to weeks

mediated by T. cells which react against the alloantigens in the graft

direct allorecognition

54
Q

chronic rejection

A

months to years

mediated by T helper cells, which secrete cytokines which stimulate cellular proliferation

indirect allorecognition

55
Q

Graft vs host disease

A

follows bone marrow transplantation. Transplanted mature T. cells recognise self tissue as foreign

56
Q

Hyperacute rejection

A

preexisting Abs against ABO, HLA, other bind to transplant tissue, then induce inflammation

57
Q

Acute rejection

A

direct allorecognition of donor MHC by recipient T cell (can lead to killing by alloreactive CD8 cells and or the induction of anti graft antibodies upon CD4 T cell activation

58
Q

Chronic rejection

A

often indirect allorecognition in which in the MHC fron the donor is presented to recipient T cells, initiating B and T cell responses against the donor tissue

59
Q

Graft vs host disease occurs when

A

The graft contains mature T cells (newly emerging T cells will be educated in the recipients thymus)

There must be some histoincompatibility (MHC or minor histcompatability antigens)

The recipient must be immunocompromised ( otherwide the transplanted cells will be destoryed)

60
Q

How could an MHC mistmatch upon HSC transplant affect T cell responses

A

You get a bone marrow transplantation and then the donor HSC reconstitutes recipients HSC system (T cells and APCs come from donor)

Positive selection in the thymus. Donor T cell sees recipient thymic epithelial cells

Recipient and donor not HLA matched

upon infection, donor APC in periphery present pathogen derived peptides to donor T cells

No adaptive immune response. Infection persists

61
Q
A

The patient had pre-formed antibodies specific for alloantigens on graft endothelial cells

62
Q
A

Immunosuppressive drugs, such as cyclosporine, are effective in preventing or treating this type of rejection

acute rejection mediated by T cells specidic for alloantigens in the heart.

Chronic is not likely at 14 weeks

63
Q
A

CD8+ lymphocytes

64
Q

Activation of tumor specific T cells specific for tumor antigens (usually tumor associated neoantigens) and the adjuvsants taht can promote and anti-tumor response

A

Problem:

Tregs

tumor evolution

65
Q

Isolation, expansion, and re-infusion of tumor infiltrating lympho cytes

A

problem

logistics

66
Q

Blocking immunosuppressive mechanisms that inhibit anti-tumor responses ( such as CTLA-4, PD-1, and regulatory T cells)

A

problem: autoimmunity

67
Q

genetically modifying T cells so that they targer tumors (CAR-T cells)

A

Problem

cytokine storm

68
Q

The use of monoclonal antibodies against tumor antigens

A

problem

anti-mab abtibodies

tumor evolution

69
Q

Autoimmunity

A

blocking T cell activation using soluable CTLA-4

involved in down regulating immune responses (T cell)

70
Q

Cancer immunotherapy

A

preventing T cell inhibition by blocking CTLA-4 or PD-1 using monoclonal antibodies

71
Q

What are chimeric antigen receptors?

A

making artificial receptor that binds to a tumor antigen

signaling domain is similar to a T cell receptor. Activated in the same way T cell is. Will kill

Advantages: many more cells specific for tumors

much higher affinity for tumor cells

72
Q

Which of the following statements about immune response to tumor is true?

T. cells specific for tumor antigens. cannot be found in most human tumor patients

Antibodies specific for tumor antigens cannot be found in many human tumor patients

The presence of lymphocytic infiltrates in certain tumors is associated with a worse prognosis than lymphocyte poor tumors of the same histologic type

immunodeficient individuals are more likely to develop certain cormas of cancer than are immunocompetent individuals

the host immune response us usually capable of eradicating common tumors once they are established

A

immunodeficient individuals are more likely to develop certain cormas of cancer than are immunocompetent individuals

infiltrating T lymphocytes good

73
Q
A

To stimulate CD8+ T lymphocytes targeting cells that express E6 and E7

E6 and E7 expressed in cytosol. Abs probably wouldnt work.

74
Q
A

It prevents costimulation of T cells by antigen presenting cells

75
Q
A

Inhibition of B cell activation by Th cells

FMS Week 9 (2 decks)

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