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Immunology > Immunology Exam 5 > Flashcards

Immunology Exam 5 Flashcards

1
Q

Most allergens are _______

A

Proteins

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2
Q

Most therapeutic antibodies used to treat cancer and other diseases are isolated from the blood of rabbits and domesticated animals such as horses and goats.
True/False

A

False

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3
Q

Hypersensitivity disorders may arise from recognition of self-antigens or environmental antigens.
True/False

A

True

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4
Q

The progression of HIV infection to AIDS is most directly due to which of the following?

A. A loss of CD4+ T cells to numbers insufficient to prevent infections
B. Reduction in CD8+ CTLs specific for HIV
C. Reduction in serum IgG levels to levels insufficient to prevent infections

A

A. A loss of CD4+ T cells to numbers insufficient to prevent infections

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5
Q

Many genes are associated with an individual’s chance of developing an autoimmune disease. Among the most important are ______ genes

A

human leukocyte antigen (HLA)

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6
Q

All of the following are effector mechanisms of antibody-mediated disease EXCEPT:
A. Complement- and Fc receptor–mediated inflammation and tissue injury
B. Antibody stimulation of cell surface receptors in the absence of the physiologic ligands
C. Death ligand-dependent apoptosis of cells
D. Opsonization and phagocytosis of cells

A

C. Death ligand-dependent apoptosis of cells

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7
Q

All of the following may result in an acquired immunodeficiency EXCEPT:
A. An inherited defect in B cell maturation
B. Malnutrition
C. Treatment with corticosteroids

A

A. An inherited defect in B cell maturation

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8
Q

Which of the following is a correct description of checkpoint blockade drugs used in tumor immunotherapy?
A. Soluble Ig-fusion proteins that contain the extracellular domains of T cell inhibitory molecules
B. Inhibitory monoclonal antibodies specific for T cell molecules that normally inhibit T cell activation
C. Inhibitory monoclonal antibodies specific for T cell molecules that normally enhance T cell activation
D. Small molecule inhibitors of JAK kinases involved in cytokine activation of T cells

A

B. Inhibitory monoclonal antibodies specific for T cell molecules that normally inhibit T cell activation

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9
Q

Histamine is a critical product of the late-phase reaction.
True/False

A

False

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10
Q

In comparison to individuals with a normal immune system, immunocompromised individuals are less likely to develop cancer.
True/False

A

False

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11
Q

Which of the following best describes the genetic basis of autoimmunity?
A. polymorphic only
B. polygenic and polymorphic
C. neither polygenic nor polymorphic
D. polygenic only

A

B. polygenic and polymorphic

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12
Q

Herceptin acts to inhibit HER2-positive breast cancer by ________

A

promoting antibody-dependent cellular cytotoxicity via NK cells

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13
Q

All of the following represent possible neoantigens (tumor-specific antigens) EXCEPT:
A. proteins coded for by tumor-causing viruses
B. amino acid substitutions in oncoproteins
C. low abundance proteins that are overexpressed

A

C. low abundance proteins that are overexpressed

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14
Q

Some cancer cells and some viruses evade the immune system by expressing IL-10 or IL-10-like proteins.
True/False

A

True

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15
Q

Which type of hypersensitivity reaction involves IgG and IgM antibodies targeting cell-surface or extracellular matrix (ECM) proteins?

A

Type 2

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16
Q

Active immunotherapies ______

A

are currently the primary focus of anti-cancer research and therapy

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16
Q

Which of the following statement describes leukocyte adhesion deficiency (LAD)?
A. LAD is a consequence of HIV infection.
B. LAD blocks the interaction of B cells and T cells.
C. LAD causes Type IV hypersensitivity.
D. LAD inhibits the crawling ability of certain innate immune cells

A

D. LAD inhibits the crawling ability of certain innate immune cells

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17
Q

All the following describe mRNA vaccines in regards to cancer EXCEPT:
A. The mRNA component of the vaccine codes for neoantigens.
B. Many clinical trials of mRNA vaccines are currently in progress.
C. These vaccines only can be used for prophylactic purposes.

A

C. These vaccines only can be used for prophylactic purposes.

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18
Q

People with allergies will generate immediate and late-phase reactions upon their first exposure to an allergen.
True/False

A

False

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19
Q

“Bystander activation” describes events associated with the ability of _____________

A

infection to induced activation of self-reactive T cells

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20
Q

Allergies represent an immune reaction to a foreign but non-pathogenic antigen
True/False

A

True

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20
Q

Mast cells, basophils, and eosinophils are components of the ______ immune system

A

Innate

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21
Q

Intestinal hypermotility has evolved to:

A

clear worms from gut

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22
Q

Autoimmune disease represent a type of hypersensitivity disorder.
True/False

A

True

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23
Q

A drug used to reduce the chance of transplant rejection might also be useful for the treatment of certain hypersensitivity disorders.
True/False

A

True

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23
Q

Onset of autoimmune disease is often associated with or proceeded by infection.
True/False

A

True

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24
Q

Following delivery to the patient, which of these active immunotherapies is the most direct means to kill cancer cells?
A. checkpoint blockade
B. phophylactic vaccination
C. cellular vaccination with DCs
D. adoptive T cell transfer

A

D. adoptive T cell transfer

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25
Q

In contributing to autoimmune disorders, polymorphisms in HLA genes are typically located in and around the antigen cleft while polymorphisms in non-HLA genes are typically located in genes are typically located in gene regulatory regions that control protein expression.
True/False

A

True

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26
Q

Passive immunotherapy utilizes mAbs that recognize proteins expressed by normal cells.
True/False

A

False

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27
Q

Which approach is more likely to induce cancer cells able to resist treatment?

A

Passive immunotherapy

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28
Q

Shortly before infusion of T cells, patients may be treated with chemotherapy drugs to ________.

A

reduce the T cell population to make “room” for the new T cells

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29
Q

Which of the following is NOT a mechanism for cancer cells to evade the immune system?
A. increased expression of soluble stress ligands
B. decreased expression of cell-surface stress ligands
C. reduced expression of MHC Class 1 proteins
D. increased expression of neoantigens

A

D. increased expression of neoantigens

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30
Q

The ability to recruit and activate Treg cells would help cancer cells evade the immune system
True/False

A

True

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31
Q

Which of the following statements about mAbs is FALSE?
A. A given mAb is able to recognize several different epitopes
B. For therapeutic use, mAbs are typically generated in mice
C. mAbs are proteins
D. Polyclonal Abs are simple a mixture of various mAbs against the same antigen

A

A. A given mAb is able to recognize several different epitopes

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32
Q

The ability to evade the immune system generally occurs _____ in the development of cancer

A

Late

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33
Q

Tumor cells present cancer antigens via _____ proteins

A

MHC Class 1

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34
Q

How does the immune system detect cancer cells as foreign?

A
  1. Cancer cells express novel peptide sequences (neoantigens or tumor-specific antigens (TSAs))
  2. Cancer cell may also overexpress normally rare
    proteins or proteins that otherwise failed to elicit
    complete tolerance (Tumor-Associated Antigens)
35
Q

Characteristics of cancer cell-specific antigens

A
  • Increase as cancer develops and cancer cell genome becomes increasingly instable
  • Consist of both passenger mutations (most) and driver mutations
  • Presented by Class I MHC molecules on tumor cells
  • May be ingested by DCs and presented by Class II MHC or cross-presented by Class I MHC
36
Q

Steps in CTL response against tumors

A
  1. Dendritic cell grabs phagocytosed tumor antigen and migrates to lymph node
  2. Activation of tumor antigen-specific CD8+ T cell through cross-presentation
  3. Migration of tumor-specific CTL to tumor
  4. CTL killing of tumor cell
37
Q

Other than CTLs, what are other responses against tumors?

A
  • Anti-tumor antibodies have been found in blood of cancer patients but impact unclear
  • Tumor antigen-specific CD4+ T cells (Th1 cells) support CTLs and macrophages via cytokines
  • Activated macrophages can kill tumor cells via NO (nitric oxide)
  • Activated NK cells can kill tumor cells that express stress ligands
38
Q

What sources of chronic inflammation promote tumors?

A

Hepatitis B and C
H. pylori
Asbestos
Obesity

39
Q

Strategies cancer uses to evade the immune system

A
  • hide identity
  • hide stress
  • inactivate immunocytes
  • avoid apoptosis
  • induce immunocyte apoptosis
  • neutralize intracellular toxins
  • neutralize complement
  • recruit Treg cells which inhibit Th and Tc cells
  • up-regulate CD47 signal (don’t eat me)
40
Q

Hide identity: mechanism and agent being evaded

A
  • Repress tumor antigen (TATA/TSTA)
  • Repress MHC class 1 proteins (not transcribed/not delivered to PM) (breast cancer does this)
  • CTLs
41
Q

Hide stress: mechanism and agent being evaded

A
  • repress NKG2D ligands (MICA)
  • NK cells (they have receptors that recognize cells expressing stress ligands)
42
Q

Inactivate immunocytes: mechanism and agent being evaded

A
  • Secrete stress ligands into environment to “distract” immunocytes
    => soluble ligand binds to receptor on immunocyte:
    1. inhibits binding to stress ligand on cancer cell, or
    2. induces endocytosis and degradation of receptor
  • NK cells, CTLs, and variety of immunocytes
43
Q

Avoid apoptosis: mechanism

A
  • inhibit capase cascade by increasing IAPs
  • acquire resistance to FasL-mediated apoptosis

*Hallmark of cancer

44
Q

Induce immunocyte apoptosis: mechanism and agent being evaded

A
  • release soluble FasL
  • release cytokines (IL-10/TGF-beta) (Epstein-Barr virus codes for modified IL-10)
  • CTLs, dendritic cells, macrophages
45
Q

Neutralize intracellular toxins: mechanism and agent being evaded

A
  • enzymatic detoxification of H2O2
  • macrophages, NK cells
46
Q

Neutralize complement: mechanism and agent being evaded

A
  • over-express mCRPs (membrane-bound complement regulatory proteins)
  • complement system
47
Q

Passive vs Active immunotherapy

A

Passive => use mAbs against neoantigens as drugs
Active => stimulate patient’s immune system to attack cancer

48
Q

Example of passive immunotherapy

A

Herceptin/Trastuzumab = monoclonal antibody against HER2 (epidermal growth factor receptor)

Mechanisms of Herceptin action:
1. Promotes antibody-dependent cellular cytotoxicity via NK cells
2. Suppresses cell survival pathways by inducing HER2 endocytosis and degradation

49
Q

Nomenclature of therapeutic monoclonal antibodies

A

Prefix + Substem A + Substem B + mab

50
Q

Which mAbs are used to activate the immune system?

A
  • Yervoy/Ipilimumab
  • Opdivo/Nivolumab
  • Keytruda/Pembrolizumab
  • Tecentriq/Atezolizumab
  • Imfinzi/Durvalumab
  • all are anti-CTLA-4/PD-1 which promotes costimulation/inhibit immune checkpoints
51
Q

Types of active immunotherapies for cancer

A
  • checkpoint blockade
  • cancer vaccines
  • adoptive T cell transfer
52
Q

What prophylactic cancer vaccines are in use for humans?

A

HPV (human-papillomavirus) and HBV (hepatitis B virus)

~ focuses on viral-induced cancers

53
Q

How do cellular cancer vaccines utilize TSA-loaded DCs?

A
  1. Isolate DCs from patient
  2. Expand Dcs in culture
  3. Activate DCs by exposure to TSAs from cancer
  4. Return activated DCs to patient
  5. DCs induce generation of CTLs that recognize TSAs
54
Q

How does adoptive T-cell transfer work?

A
  1. Isolate T cells from patient
  2. Expand in culture
  3. Incubate with tumor cells or TSA-loaded APCs
  4. Infuse activated, cancer-specific T cells
55
Q

How does chimeric antigen receptor (CAR) T cell therapy work?

A
  1. Identify neoantigen on patient’s cancer cells
  2. Raise antibody against this antigen
  3. Use rDNA to create CAR
  4. Introduce CAR gene into T cells
  5. Infuse CAR-T cells into patient

~works best with blood cancers

56
Q

Why is CAR T cell therapy considered a “double-edged sword”?

A

The therapy eliminates the need for APCs and MHC/antigen displaying and signaling, but it can induce a cytokine storm.

57
Q

What are autoimmune disorders associated with?

A
  • loss of self tolerance
  • abnormal display of self antigens
  • inflammation/innate imune response
58
Q

Mechanisms of loss of self tolerance

A
  • Failure to delete or inactivate self-reactive lymphocytes, and/or
  • Activation of APCs so self-antigens are presented in immunogenic manner
59
Q

Mechanisms of abnormal display of self antigens

A
  • Increased expression or persistence of self antigens, or
  • Structural changes in self antigens due to stress/injury (neoantigens)
60
Q

How does self tolerance fail?

A
  • genetic susceptibility
  • epigenetic changes
61
Q

How are self reactive lymphocytes activated?

A
  • environmental triggers recruit & activate self-reactive lymphocytes that may alter self-antigen display
  • microbiome changes
62
Q

Role of infection in autoimmunity

A
  1. Bystander activation: microbes activate APCs to express co-stimulators, which can activate self-reactive T cells
  2. Molecular mimicry: peptide similarity between microbial antigen and self antigen activates T/B cells that recognize self antigen.
63
Q

What are hypersensitivity disorders a results of?

A

Result from tissue damage due to unchecked or inappropriate immune responses

64
Q

What are the specific antigens the initiated hypersensitivity disorders?

A
  1. Self antigens => lead to autoimmune diseases
  2. Microbial antigens from persistent infections => antibody- or T cell-dependent damage
  3. Non-microbial environmental antigens => allergic disorders
65
Q

What is the classification of hypersensitivity disorders?

A

Based on type of immune response and main damage-inducing effector mechanism
- Type 1: immediate
- Type 2: antibody-mediated
- Type 3: immune complex-mediated
- Type 4: T cell-mediated

65
Q

What is immediate (type 1) hypersensitivity?

A
  • allergies
  • caused by antibodies specific for environmental antigens
66
Q

What is antibody-mediated (type 2) hypersensitivity?

A
  • Due to IgM and IgG specific for cell surface or ECM antigens (organ-specific)
  • Effector mechanisms
    1. Opsonization and phagocytosis kills host cells
    2. Complement- and Fc receptor-mediated inflammation and injury
    3. Inhibition of cell / tissue functions without injury (e.g., NT receptor)
67
Q

What is immune complex-mediated (type 3) hypersensitivity?

A
  • Due to IgM and IgG specific for soluble antigens in blood (systemic)
  • Antigen may be either self or foreign antigen
    => Occurs in individuals who receive therapeutic antibodies produced in animals
  • Complexes activate complement and recruit leukocytes via Fc receptors
  • Leads to inflammation, thrombosis, and injury
68
Q

What are the therapeutic interventions fro hypersensitivity diseases?

A
  • Broadly acting anti-inflammatory agents ( corticosteroids, NSAIDs)
  • Anti-cytokine therapies
  • Depletion of certain immune cells and antibodies
  • Specific biologic agents
  • Tolerance-inducing therapies
68
Q

What is T cell-mediated (type 4) hypersensitivity?

A

Cytokine-mediated inflammation via CD4+ helper T cells
=> cytokines recruit neutrophils and macrophages
* CTLs kill cells and damage tissue

69
Q

What do broadly acting anti-inflammatory agents do?

A

inhibit cytokine secretion

70
Q

What do anti-cytokine therapies do?

A

bind to and inhibit specific cytokines or cytokine receptor pathways

71
Q

What does depletion of certain immune cells and antibodies do? (hypersensitivity)

A
  • monoclonal Abs that deplete lymphoid cells, only B cells, or only T cells
  • plasmapheresis can remove autoantibodies and immune complexes
72
Q

What do specific biologic agents do? (hypersensitivity)

A
  • CTLA-4-Ig blockade of the B7 co-stimulator pathway
  • Anti-integrin Abs Inhibit leukocyte migration
73
Q

What do tolerance-inducing therapies do?

A
  • Deliver known antigen while inhibiting lymphocytes specific for the antigen
  • Activate or infuse Tregs
74
Q

Sequence of events in immediate hypersensitivity

A
  1. first exposure to allergens
  2. activation of Tfh cells and stimulation of IgE class switching in B cells
  3. production of IgE
  4. binding of IgE to FcR on mast cells (now sensitized)
  5. Repeat exposure to allergen
  6. activation of mast cell: release of mediators
    7a. vasoactive amines, lipid mediators –> immediate hypersensitivity reaction
    7b. cytokines –> late-phase reactions (2-4 hours after)
75
Q

Steps in mast cell activation

A
  1. IgE-coated resting mast (high-affinity receptor)
  2. Antigen-cross-linked IgE-FcRI triggers signal cascade to activate mast cell
    3a. Degranulation releases hydrolases, proteases, vasoactive amines (histamines), and lipid mediators.
    4a. vascular and smooth muscle response: immediate reaction
    3b. cytokines are synthesized
    4b. inflammation: late phase reaction
76
Q

What are the mediators of immediate hypersensitivity reaction?

A

Vasoactive amines (histamines)
- relaxation of vascular smooth muscle
- leakage between epithelial cells

Protease
- local tissue damage

Lipid mediators
- bronchoconstriction
- leukocytes (inflammation)

77
Q

What are the mediators of late phase hypersensitivity reaction?

A

Cytokines
- inflammation

Eosinophils
- recruitment and activation

78
Q

Primary vs secondary immunodeficiency

A

Primary
- congenital/genetic defect
- become apparent in infancy or early childhood

Secondary (more common)
- acquired/not inherited
- May result from malnutrition, some cancers, immunosuppressive drugs or infection of immune cells

79
Q

What is leukocyte adhesion deficiency (LAD)?

A
  • Innate immune immunodeficiency
  • mutations in leukocyte or endothelial adhesion molecules (integrins/ligands)
  • causes failure of leukocytes to move to the site of infection
80
Q

What are severe combined immunodeficiencies (SCIDs)?

A
  • Impaired T cell development
  • May involve defects in B cell development
    **if not humoral defects still occur bc of helper T cell failure
  • cause severe infections by various pathogens
81
Q

Progression (phases) of untreated HIV infection

A
  1. Acute phase
  2. Transition phase
  3. Chronic (clinical latency) phase
  4. AIDS
82
Q

Describe the acute phase of an HIV infection

A
  • infection of activated CD4+ T cells in mucosal epithelia
  • death of most local infected CD4+ T cells within two weeks
83
Q

Describe the transition phase of an HIV infection

A
  • Dissemination of virus via – - DCs to lymph nodes
  • Transfer of virus to node CD4+ T cells
  • Viral replication => “viremia”
  • Spread of CD4+ cell infection throughout body
  • Adaptive immunity response to virus => partial control
84
Q

Describe the chronic phase of an HIV infection

A
  • Infection and cell death limited to lymphoid tissues
  • Immune system still able to control other infections
  • CD4+ T cell numbers decline over years
85
Q

Describe the AIDS phase of an HIV infection

A
  • CD4+ T cell numbers drop below functional level
  • Opportunistic infections
  • Cancer
  • Cachexia
  • Organ failure
86
Q

Main treatment for

A

Two different reverse transcriptase inhibitors + a protease inhibitor

Immunology (2 decks)

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