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Immunology > Immunology Exam 4 > Flashcards

Immunology Exam 4 Flashcards

Test Review

1
Q

Donor APCs can present donor peptides to host T cells.
True or False

A

True

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2
Q

CD8+ CTLs provide the primary response to extracellular bacteria.
True or False

A

False

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3
Q

Antigenic shifts in certain viruses are associated with _____________

A

reassortment of the RNA genome

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4
Q

Surgery associated with tissue or organ transplantation would be expected to lead to generation of _________, which activate an innate immune response.

A

DAMPs

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5
Q

An allogeneic graft is between ________________

A

two individuals of the same species

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5
Q

Regardless of type of infectious microbe, _____________ is generally the major contributor to immune-dependent host damage.

A

Inflammation

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6
Q

Humans express natural antibodies that recognize A or B blood antigens and xenogeneic tissue in the absence of any previous exposure to such antigens or tissue.
True or False

A

True

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7
Q

Parasite infections ____________

A

Often chronic

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8
Q

Which of the following statements about the antiviral state is FALSE?
A. The antiviral state may damage or kill host cells.
B. The antiviral state reduces the spread of virus to other host cells.
C. The antiviral state serves to destroy existing virus particles.

A

C. The antiviral state serves to destroy existing virus particles.

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9
Q

Blockage of blood vessels by proliferating smooth muscle cells is typically associated with ___________ allograft rejection

A

Chronic

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10
Q

Viruses are able to _________.
A. reproduce in the extracellular environment
B. induce many cells to express Type I interferons
C. simply diffuse across the plasma membrane of any host cell

A

B. induce many cells to express Type I interferons

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11
Q

The rejection of a transplanted organ or tissue by the recipient’s immune system is primarily mediated by _________.

A

T cells

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12
Q

Antigenic drift is typically associated with _________

A

Point mutations

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13
Q

Some viruses code for proteins that are similar to cytokines or that bind to cytokines.
True or False

A

True

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13
Q

Which drug inhibits T cell activation by blocking the calcineurin pathway?

A

Cyclosporine

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13
Q

Which of the following is a mechanism by which immunosuppressive drugs may help treat or delay graft rejection?
A. activation of B7-mediated costimulation
B. decreased production of IL-2
C. increased proliferation of T lymphocytes

A

B. decreased production of IL-2

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14
Q

In the time course of an immune response to viral infection, Natural Killer cells will become active before CTLs become active.
True or False

A

True

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15
Q

Which of the following strategies would allow a virus to evade or resist the host immune response?
A. Increased expression of MHC Class II proteins
B. Inhibition of proteasome activity
C. Activation of TAP transport

A

B. Inhibition of proteasome activity

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16
Q

All of the following describe fungal infections EXCEPT:
A. Antibodies can defend agains fungal infections.
B. Fungal infections may be opportunistic.
C. Macrophages and neutrophils can defend against fungal infections
D. Fungal infections may be extracellular but can’t be intracellular.

A

D. Fungal infections may be extracellular but can’t be intracellular.

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17
Q

The process by which the transplanted tissue attacks the recipient’s tissue is termed:

A

Graft-versus-host disease (GVHD)

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18
Q

Chronic rejection is primary associated with vascular occlusion by ______.

A

smooth muscle cells

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19
Q

The immune system can recognize and kill cancer cells.
True or False

A

True

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20
Q

Drugs that suppress the immune system can also be used to treat cancer.
True or False

A

True

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21
Q

Alloreactive antigens may be presented to the recipient’s T cells by wither donor DCs or recipient DCs.
True or False

A

True

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22
Q

The problem of hyperacute rejection is most effectively dealt with by:

A

screening for ABO blood type

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23
Q

Treatment to reduce or delay transplant rejection will increase the risk of infection for the recipient.
True or False

A

True

24
Q

Alloantigens are:

A

MHC proteins

25
Q

The _____ mechanism by which alloreactive T cells recognize alloantigens is most like the mechanism used by T cells to detect pathogens.

A

Indirect

26
Q

The “anti-viral” state ______.

A

inhibits virus replication and assembly

27
Q

What evasion mechanisms does SARS-CoV-2 exhibit?

A

Undergo antigenic variation and infect other animals

28
Q

T cell-mediated response to intracellular fungi depends on expression of _____ by the infected cell.

A

MHC class 1 proteins

29
Q

Type 1 IFN expression is most likely the result of _______ activation.

A

pattern recognition receptor

30
Q

What is the main innate immune response against viral infections?
What is the main adaptive immune response against viral infections?

A
  • Type 1 interferon to induce the antiviral state.
  • B cell secretion of antibodies
31
Q

What do antibodies do to viral antigens?

A
  • block binding of virus to its receptor
  • opsonize –> phagocytosis
  • effective only against extracellular particles
  • prevent cell-to-cell spread and re-infection
32
Q

Steps of cytokine-induced antiviral state.

A
  1. Production of Type 1 IFN by viral infected cell. IFN binds to an IFN receptor on an uninfected cell.
  2. IFNs induce expression of enzymes that block viral replication.
    - inhibition of viral protein synthesis
    - degradation of viral RNA
    - inhibition of viral gene expression and virion assembly
33
Q

Other than antiviral state, what does IFN also induce?

A
  • favor lymphocyte retention in nodes
  • enhance NK and CTL activity
  • up-regulate class 1 MHC proteins
34
Q

What two cells are responsible for killing of virus-infected cells?

A

NK cells and CD8+ CTLs

35
Q

Explain antigenic shift.

A

Genetic recombination of two viral strains

Less frequent than antigenic drift
=> but more sudden and significant change

Simultaneous infection by two strains
allows for reassortment of RNA strands

35
Q

Explain antigenic drift.

A

Results from point mutations that either:
* accumulate throughout the antigen over time (minor changes add up)
* occur in key antigenic site (major change)

36
Q

Ways of inhibition of antigen processing and class 1 MHC presentation.

A
  • inhibition of proteasomal activity
  • block in TAP transport
  • block in MHC synthesis and/or ER retention
  • removal of class 1 from ER
  • engagement of NK cell inhibitory receptors by “decoy” viral class 1-like molecules
37
Q

Mechanisms viruses use to evade the immune system.

A

Coding for proteins that:
* Act as ligands for NK cell inhibitory receptors
* Function as decoy signal molecules that compete with cytokines
* Resemble immunosuppressive cytokines such as IL-10
* Bind to and inhibit pro-inflammatory cytokines

Exhaustion of CTLs cells

Killing or inactivation of immune cells

38
Q

Immunity against intracellular pathogens.
a. Effector T cell:
b. Cytokines:
c. Target cell:
d. Immune reactions:
e. Diseases it can cause:

A

a. Th1
b. IFN-gamma
c. macrophages
d. macrophage activation
e. autoimmunity and chronic inflammation

39
Q

Immunity against helminths pathogens.
a. Effector T cell:
b. Cytokines:
c. Target cell:
d. Immune reactions:
e. Diseases it can cause:

A

a. Th2
b. IL-4, IL-5, IL-13
c. eosinophils
d. eosinophils and mast cell activation
e. allergies

40
Q

Immunity against extracellular pathogens.
a. Effector T cell:
b. Cytokines:
c. Target cell:
d. Immune reactions:
e. Diseases it can cause:

A

a. Th17
b. IL-17 and IL-22
c. neutrophils
d. neutrophil recruitment and activation
e. autoimmunity and inflammation

41
Q

What is the main innate immune response against extracellular bacteria infections?
What is the main adaptive immune response against extracellular bacteria infections?

A

Innate immune response: complement, phagocytosis, inflammation

Adaptive immune response: antibody-dependent neutralization & opsonization

**May induce cytokine-mediated, inflammatory damage to host

42
Q

What is the main innate immune response against intracellular bacteria infections?
What is the main adaptive immune response against intracellular bacteria infections?

A

Innate immune response: phagocytes and NK cells

Adaptive immune response: CD4+ T cells activate phagocytes to kill microbes

**May result in macrophage-associated damage

43
Q

What is the main innate immune response against fungi infections?
What is the main adaptive immune response against fungi infections?

A

Innate immune response: neutrophils and macrophages

Adaptive immune response: humoral (extracellular), T cell-mediated (intracellular)

44
Q

What is the main innate immune response against parasite infections?
What is the main adaptive immune response against parasite infections?

A

Innate immune response: phagocytosis (protozoa), inflammation (helminths)

Adaptive immune response: varied humoral and cell-mediated

45
Q

Innate immune responses to grafts

A
  1. procedure
  2. ischemic damage (reduced blood and oxygen supply)
  3. cell dysfunction and death
  4. DAMPs produced in graft
  5. innate immune responses by host and donor cells
  6. Some innate responses directly kill donor cells
    Some activate APCs to promote adaptive responses
45
Q

Adaptive immune response to grafts (primary reason for rejection)

A

Alloantigens induce both cellular and humoral immune responses

MHC molecules are:
* most important alloantigens responsible for strong and rapid transplant rejection
* so polymorphic that no two individuals will inherit the same ones

46
Q

Steps in direct alloantigen recognition.

A
  1. T cells recognize donor MHC and bound peptides on DC from graft
  2. Effector CD8+ T cell recognizes donor MHC on graft tissue cell
  3. Direct CTL killing of graft cells
47
Q

Steps in indirect alloantigen presentation

A
  1. Recipient DC takes up and processes donor MHC molecules.
  2. CD4+ T cell recognizes donor MHC peptide bound to recipient MHC on recipient DC.
    3a. Effector CD4+ T cell recognizes donor MHC peptide bound to recipient MHC on recipient B cell
    3b. Effector CD4+ T cell recognizes donor MHC peptide bound to recipient MHC on recipient macrophage in graft
    4a. Antibody-mediated injury to graft cells
    4b. Inflammation-mediated injury to graft.
48
Q

Activation of alloreactive T cell - sensitization

A
  1. From allograft, transportation of alloantigens to lymph node.
  2. Activation of T cells , generation of effector T cells by direct and indirect antigen presentation
49
Q

Activation of alloreactive T cell - rejection

A
  1. Killing of graft tissue cell
  2. Cytokine secretion
  3. Activation of effector T cells by alloantigen; graft rejection
  4. Migration of effector T cells to allograft
50
Q

Explain hyperacute rejection.

A
  • Existing host Abs bind endothelial cells and activate complement
  • Damage induces clotting, vessel occlusion, thrombosis, and ischemic cell death
  • Happens with blood transfusions
51
Q

Explain acute cellular rejection.

A

Principal causal mechanisms are:
* CTL-mediated killing of graft
parenchymal cells and endothelial cells
* inflammation triggered by helper T cell-produced cytokines

52
Q

Explain acute antibody-mediated rejection.

A
  1. Alloantibodies bind to
    alloantigens (mainly MHC)
    on vascular endothelial cells
  2. Complement activation,
    Fc receptor engagement
  3. Inflammation,
    Endothelial cell death,
    Blood clot formation
52
Q

Explain chronic rejection.

A
  1. Activation of alloreactive T cells, secretion of cytokines.
  2. Stimulates proliferation of
    vascular smooth muscle cells
  3. Vascular occlusion blocks
    blood flow to parenchyma
  4. Organ failure
53
Q

Mechanisms of action of immunosuppressive drugs

A
  • Delay or treat graft rejection
  • Act to inhibit or kill T lymphocytes
  • Fall into certain categories that
    target either cell surface or
    intracellular proteins
54
Q

What does cyclosporine do?

A

Shutdown of IL-2 signaling by inhibiting IL-2 transcription and inhibiting calcineurin.

55
Q

What does rapamycin do?

A

Rapamycin inhibits mTOR kinase
- mTOR promotes cell survival & proliferation in response to IL-2R and TCR activation

56
Q

What do antimetabolites do?

A

Toxins that poison T cell proliferation by various mechanisms

57
Q

Consequences of ABO mismatch.

A

Pre-existing IgMs bind to “foreign” antigen on donor cells
=> activate complement in vasculature
=> induce phagocytosis via opsonization in liver and spleen

Resulting hemolysis of RBCs releases large amount of hemoglobin
=> toxic to kidneys

Innate response = fever, shock, disseminated coagulation via cytokine storm

Reactions are generally serious and may be fatal

Immunology (2 decks)

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