immune defenses Flashcards

1
Q

What is the purpose of the invariant chain?

A

It prevents peptides in the ER from binding on MHC II before they reach the endosome which contains extracellular proteins

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2
Q

What can kill multiple virus-infected cells?

A

CD*+ cytotoxic t cells

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3
Q

What must also bind for Cyt. T cell activation?

A

Coreceptors ust bind as well. They facilitate adhesion of the two cells together

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4
Q

The MHC-peptide complex interacting with CD receptor is ____ in the chain of T-cell activation

A

signal 1

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5
Q

how can virus affect T cell activation?

A

They can affect structure, function of T cell receptors. MHC can be downregulated in the cell

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6
Q

How does a cyt. T cell work?

A

Release of perforins and granzymes

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7
Q

Perforin makes holes in _____ ____ . What do granzymes do? How long does it take?

A

endosomal membrane; cleave caspases to activate them; minutes

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8
Q

How long does it take for CTL activity appear?

A

3-5 days, peaking 1 week in

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9
Q

If CTLS from an infected organism are transferred to a non-immunized recipient, can they protect them?

A

Yes they can

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10
Q

Some immunopathology often follows infection by noncytopathic virus. Why?

A

CTLs kill infected cells. Ex: hepatitis

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11
Q

Activating signal of B cells requires ___ of receptors complexed with antigen

A

clustering

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12
Q

B cells have MHC II receptors in order to

A

Present antigens to Th2 helper cells in order to stimulate more cytokines for B cell stimulation

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13
Q

VL stands for:

A

Variable region of the light chain (antibody structure)

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14
Q

Fc stands for:

A

Fragment crystallizable (antibody structure)

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15
Q

How long of the half life of IgG?

A

7 to 21 days

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16
Q

How long can specific IgG molecules be detectable in the body

A

years due to memory B cells

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17
Q

IgG and IgM are important for ____ infections

A

viremic

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18
Q

Immunodeficient animals can be protected from lethal viral infections by injection with ___ ____ ____ or monoclonal antibodies

A

virus-specific antiserum (passive immunization)

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19
Q

Poliovirus infection stimulates strong IgM and IgG response in blood, but ____ __ is vital for defense

A

mucosal IgA

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20
Q

What makes IgA?

A

Plasma cells in mucosal epithelium

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21
Q

What is the primary mechanism of antibody-mediated viral neutralization?

A

steric blocking of virion-receptor interaction

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22
Q

Antibodies can also promote aggregation of virions, what does this accomplish?

A

It reduces the effective concentration of infectious particles.

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23
Q

A negative effect of antibody can be that they ____ ____

A

enhance infectivity. Antibody bound to virions is recognizing by Fc receptors on macrophages, which allows it to enter the cell by endocytosis.

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24
Q

What is another way that antibody can affect virus, especially during endocytosis?

A

Antibodies can prevent capsid uncoating

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25
Q

What starts from a single infected cell?

A

The cascade of antiviral defense

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26
Q

If viral replication isn’t slowed after the cascade begins, what is then activated?

A

The immune defense

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27
Q

What are the three steps of the immune defense?

A

recognition, amplification, and control. It is also critical that it is stopped after the infection has abated.

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28
Q

When is the innate immune response activated? What are its components?

A

When the intrinsic defenses of the cells and tissue are unable to stop the infection; cytokines released from infected cells, local sentinel cells (dendritic cells and macrophages), the complement system, NK cells

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29
Q

What WBC cells are of lymphoid origin?

A

T cells, B cells, NK cells,

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30
Q

What WBC cells are of myeloid origin?

A

monocytes, dendritic cells, and neutrophils

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31
Q

Where is MHC II located on an immature dendritic cell? Toll-like receptors? cytokine receptors?

A

MHC II is located in endosomes. TLRs are on the exernal plasma membrane, as well as cytokine receptors

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32
Q

Where is MHC II located on a mature dendritic cell? Mature dendritic cells secrete ______ _____ in order to activate ___ cells

A

on the cell surface; proinflammatory cytokines; T

33
Q

NK cells secrete ____, _____, and ____, _____ upon binding with a non-self MHC I molecule or MHC I without the proper protein

A

perforin, granzymes; TNF-alpha, IFN-gamma

34
Q

How does the concentration of NK cells change with response to a viral infection?

A

The number of NK cells increases exponentially after infection, and then gradually decreases once the adaptive immune response kicks in.

35
Q

How do granzymes kill a cell?

A

The activate caspase-mediated cell death.

36
Q

The activating signal of a NK cell is delivered when an NK cell receptor binds and identifies a ____ _ _____ instead of binding the _____

A

MHC I molecule; peptide

37
Q

What methods do virus use to modulate NK cell response?

A
  1. Inhibition by a viral protein with homology (similarity) to cellular MHC class 1
  2. Inhibition of expression of HLA-A or HLA-B, upregulation of HLA-E
  3. Release of virus-encoded cytokine-binding proteins that block NK-cell activating cytokines.
  4. Inhibition of action of NK cell stimulating cytokines by binding these or by producing a chemokine antagonist
  5. New virions can engage the cell, block inhibitory NK cell receptor, or infect the NK cell.
38
Q

What are HLA-A and HLA-B

A

MHC I human homologs

39
Q

When are cytokines produced? What is the multifunctionary “early warning” cytokine? What are some of its functions?

A

Cytokines are produced when certain intrinsic defenses are activated; Tnf-alpha (produced by monocytes and macrophages); capillary changes that attract and facilitate entry of circulating WBCs, antiviral response in infected cells, inducing apoptosis of infected cells within seconds of TNF-a binding

40
Q

What are the two major classes of lymphocytes? Where do T cells mature? What makes up the cell-mediated response?

A

T cells and B cells; the thymus; T cells and cytokines

41
Q

What do immature T cells mature into?

A

Cytotoxic T cells and Helper T cells (both are effector T cells)

42
Q

Where are B cells derived from? What response are they responsible for? What do they turn into?

A

Bone marrow; humoral response; plasma cells

43
Q

How is the humoral response activated?

A

The humoral response is activated when an antigen binds the antibody on the B cell surface, prompting it to undergo differentiation into plasma cells

44
Q

How is the cell-mediated response activated?

A

An antigen binds to a T cell receptor on a naive Cyt. T cell, causing it to kill the infected cell, or in the case of the helper t cell, to release Th cytokines 1 and 2, which promotes differentiation of T cells and B cells, respectively.

45
Q

What are the two cell groups the adaptive response relies upon?

A

the adaptive response relies upon lymphocytes and antigen presenting cells.

46
Q

Where do lymphocytes tend to settle?

A

Various lymphoid organs throughout the body

47
Q

If lymph nodes are removed, how does this effect adaptive immunity?

A

Without lymph nodes, the immune response will not be activated.

48
Q

What are lymphoid tissues the sites of?

A

They are the sites of communication, and collection, for cells in the circulatory system.

49
Q

What happens to T and B cells that react against self proteins?

A

They die during early maturation

50
Q

When T and B cells are made and mature, what do they do?

A

They lie in a dormant state in lymphoid tissues unless activated by the particular antigen or epitope that they protect against.

51
Q

What do APC cells do?

A

They move back and forth from tissues to the lymphoid tissues.

52
Q

What are lymph nodes the location of?

A

exchange of information between dendritic cells and lymphocytes

53
Q

M cells are found where? What is their function?

A

in the submucosal epithelium of the GI tract. They function to allow transfer of antigen from intestinal lumen to lymphoid tissue. They have pockets filled with Th cells B cells macrophages and dendritic cells

54
Q

What receptor would an infected cell display viral proteins on?

A

MHC I

55
Q

What alternative immune activity do keratinocytes display?

A

They are able to phagocytose pathogens which they can display on MHC II receptors. they also secrete pro- inflammatory cytokines

56
Q

How are T and B cell antigen receptors formed?

A

somatic gene rearrangement during organism development

57
Q

What are the functions of lymphocytes?

A

They are responsible for specificity, memory, self/nonself discrimination

58
Q

Why are T and B cells said to be naive?

A

They are naive when their specific receptor has not bound antigen, so they haven’t completely differentiated to produce their ultimate immune effector response

59
Q

The initial encounter with any foreign epitope involves only a few cells . The frequency of B or T lymphocytes that can recognize an infected cell is between:

A

1:10,000 to 1:100,000

60
Q

How long does it take for the initial response to be fully amplified? what is the increase in virus-specific lymphocyte concentration?

A

1-2 weeks. 1000X

61
Q

What is a lymphocyte that has been exposed to antigen called?

A

activated and fully differentiated.

62
Q

When an activated lymphocyte undergoes mitosis, what specific quality to the progeny share?

A

They encode for the same specific immune reactivity as the parent cell.

63
Q

Where are B cells produced? What does a B cell produce as it matures?

A

bone marrow; specific receptor which is a membrane bound antibody

64
Q

When an antigen binds specifically to a membrane-bound antibody, what ensues? A _____ ______ cascade

A

signal transduction cascade; the cell divides rapidly

65
Q

What are produced when a B cell begins to divide?

A

plasma cells and memory B cells

66
Q

What is the life span of a plasma cell? What is the maximum rate of antibody secretion?

A

a few days; more than 2000 antibodies/second

67
Q

The memory of previous infections is what made the development of _____ possible.

A

vaccines

68
Q

When encountering a virus that the organism has previously been exposed to, a ferocious adaptive response can occur within ____ of exposure

A

hours

69
Q

T-cell precursors are produced in the ____ ____

A

bone marrow

70
Q

How can T-cells be distinguished from other lymphocytes?

A

The presence of a T-cell receptor on their surface

71
Q

What are the types of T cell selection?

A

Positive selection involves selecting T cells that bind appropriate MHC surface molecules via TCR. Negative selection weeds out T cells that bind self peptides

72
Q

What are the three types of cells a naive T cell can differentiate into?

A

Cytotoxic T cells, helper T cells, and memory T cells

73
Q

How would you compare the peptide binding site of the TCR and the epitope binding site of the B cell receptor? How is this structure formed? What is another name for this region?

A

They are similar structures. They are formed by folding of the three regions in the amino-terminal domains of proteins that participate in antigen recognition; the hypervariable region

74
Q

What is the process of T cell maturation?

A

Immature T cells are – (double neg.) They differentiate sequentially in thymus, producing both CD4 and CD8 ++. Afterwards, they begin to just produce one type +, and are now “naive T cells”, and migrate to peripheral sites.

75
Q

Th cells are generally able to interact with cells with which receptors on their surface? After this interaction, what do they mature into?

A

MHC Class II; Th1 and Th2 cells

76
Q

What proinflammatory cytokine secreted by Th cells is important for viral infections? Which T helper cell would secret this, and which adaptive response would this encourage?

A

IL-12; Th1; cell mediated response

77
Q

What does cytokine IL-4 do?

A

IL-4 induces naive Th0 cells to become Th2 cells

78
Q

Viral proteins can take advantage of Th1-Th2 balance. For example, when Epstein-Barr Virus infects B cells, it encodes a ____ homolog that suppresses the Th1 response. What are the advantages of this for the virus?

A

IL-10 (vIL-10); This causes the cell to foil the Th1 defense that would help with cell-mediated defense, and also causes B cells to differentiate, which is vital to the virus’ survival