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Microbiology and Immunology > Self Non-Self Discrimination > Flashcards

Self Non-Self Discrimination Flashcards

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1
Q

What is tolerance?

A

mechanism by which lymphocytes with self-antigens are either removed or controlled

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2
Q

Where are central tolerance mechanisms active?

A

Where the lymphocyte is devloping: thymus for T cells and bone marrow for B cells

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3
Q

Where are peripheral tolerance mechanisms active?

A

secondary lymphoid tissue (nodes; adaptive response) or peripheral tissues (reaction or trigger)

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4
Q

What are the two types of tolerance?

A

central and peripheral

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5
Q

What are the mechanisms used to induce tolerance?

A

delete: eliminate the cell
anergize: turn off the cell
ignore: ignore the trigger
regulate: contain the problem (Tregs)

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6
Q

Tregs are a subset of

A

T helper/CD4+ T cells

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7
Q

What are the mechanisms of central B cell tolerance?

A

Deletion and anergy

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8
Q

What are the mechanisms of peripheral B cell tolerance?

A

Ignorance, anergy, death (lack of co-stimulation/T cell help)

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9
Q

T/F B cell tolerance is less efficient than T cell tolerance

A

True

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10
Q

Why is B cell tolerance less efficient than T cell tolerance?

A

it’s common to identify self-Ag Abs in normal healthy people - ie in diagnosing viral infections; they tend to be transient

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11
Q

B cell tolerance occurs

A

in the bone marrow during development

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12
Q

Normal mature B cells are produced from

A

non-self-reacting immature B cells that appropriately express Ag receptors on the cell surface (ie no cross-linking)

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13
Q

Clonally ignorant B cells result from

A

Immature B cells with low-affinity binding for self-antigens that is not strong enough to initiate cross-linking that activates the molecule tf it matures but does not react to its Ags

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14
Q

Anergic B cells result from

A

soluble self-molecules (eg serum proteins) with inefficient cross linking that is still able to trigger the cell; this inappropriate activation turns the cell off (anergy)

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15
Q

B cell apoptosis occurs in tolerance when

A

Multivalent self-molecules (eg membrane associated ones) cross link extensively with self antigens, inducing cell death by clonal deletion or receptor editing

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16
Q

The major peripheral tolerance mechanism for B cells is

A

survival signals

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17
Q

What are the 2 survival signals for mature B cell response and survival?

A

Signals via the surface Ig-Ag interaction (cross-linking) and T cell help (CD40L and some cytokines)

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18
Q

Affinity maturation and isotype switching are dependent on

A

T cell help, esp CD4+T cells with CD40L

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19
Q

Peripheral B cell tolerance is dependent on

A

T cell tolerance functioning, because CD4+ T cell help is required for affinity maturation and isotype switching

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20
Q

B cells see

A

whole proteins or components or whole proteins or pathogens

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21
Q

T cells see

A

peptide fragments that are processed and presented at the cell surface by MHC

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22
Q

T/F TCR only recognises peptide fragments

A

False; it also recognizes the MHC - it interacts with the complex of protein fragment and MHC

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23
Q

Why is there a ‘fine balance’ between auto-reactivity and pathogen-specific reactivity in T cells?

A

because TCRs recognize MHCs, they are self-reactive to a degree - they see self-antigen (MHC)

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24
Q

What is positive selection?

A

Thymocytes that express TCRs that recognize self-MHC are selected to survive

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25
Q

What is negative selection?

A

Removal of immature lymphocytes that have strong reactivity to self-peptide

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26
Q

Which lymphocytes survive positive selection?

A

thymocytes with TCRs that can recognize self-MHC

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27
Q

Negative selection terminates

A

immature lymphocytes with TCRs that see self-MHC w/self-peptide too well

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28
Q

AIRE

A

autoimmune regulator of expression

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29
Q

What is the function of AIRE?

A

it non-specifically turns on gene expression in the thymus of peripheral tissues and their antigens (eg insulin/pancreas) such that immature T cells get exposure to these self-Ags and can be deleted

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30
Q

Where is AIRE expressed?

A

medullary epithelial cells of the thymus

31
Q

What is the consequence of defects in AIRE?

A

failure of negative selection for some self-Ags resulting in autoimmunity

32
Q

What are the central tolerance mechanisms for T cells?

A

Deletion (main); selection of Tregs (type of CD4+T cell)

33
Q

What are the peripheral tolerance mechanisms for T cells?

A

Deletion, anergy, ignorance, and regulation

34
Q

T/F Positive selection = tolerance

A

False; it is more a mechanism of self restriction that is part of tolerance

35
Q

What are the 2 signals required for T cell activation?

A

recognition of MHC-peptide by the TCR; costimulation eg CD28 (T cell) ligating CD80/86 on DCs (upregulated by DC ligation of PAMPs - NOD, TLR, etc.)

36
Q

How does anergy arise in peripheral T cell tolerance?

A

Failure of Signal 2: costimulation (CD28 on T cell w/ CD80/86 on DC)

37
Q

What happens without Signal 2 in T cell activation?

A

failure to proliferate, inactivation (anergy), and tolerance

38
Q

Treg cells can suppress

A

all T helper cell and CD8+ T cell responses

39
Q

nTregs

A

natural Tregs - derived from thymus during T cell development

40
Q

iTregs

A

induced Tregs - derived following activation of naïve CD4 T cells in the presence of TGFb

41
Q

How do iTregs suppress autoreactivity?

A

expression of immunosuppressive cytokines IL-10 and TGFb; expression of CTLA4, an inhibitory receptor; release of suppressive molecules

42
Q

How does CTLA4 (iTregs) work?

A

CTLA4 also binds CD86 on DCs with higher affinity than CD28; this inhibits co-stimulation (signal 2) and tf activation of naïve T cells

43
Q

Autoimmune disease is defined by

A

loss of tolerance

44
Q

How is tolerance lost?

A

Self-reactive T or B cells escape regulatory mechanisms (they are deficient)

45
Q

What are the 3 key components necessary in pathogenesis of immune disease?

A

genetic susceptibility
environmental factors
loss of self-tolerance

46
Q

How can ignorance (tolerance) be lost?

A

Ag becomes available or something that looks like it that is a self-Ag that triggers the response causing these quiescent cells to become self-reactive

47
Q

How can anergy be lost?

A

if signal 2 somehow becomes supplied, autoreactive T and B cells can be activated and trigger autoimmunity

48
Q

How can peripheral B cell tolerance be lost?

A

CD4+ T cell help is provided from elsewhere, eg co-infection with viruses etc - thought to be why these trigger some autoimmune diseases

49
Q

T/F Autoimmune responses always result in autoimmune disease

A

False; they do not always result in AI disease

50
Q

T/F All autoimmune diseases involve autoimmune responses

A

True

51
Q

Autoimmunity results from

A

a chronic/ongoing autoimmune response with ongoing tissue damage

52
Q

What are the 2 classes of autoimmune disease?

A

Organ specific

Systemic

53
Q

Organ-specific autoimmune diseases are

A

confined to particular organs or cell types and the Ags recognized are organ specific

54
Q

Examples of organ specific autoimmunity are

A

thyroid, ovarian, islet cells, gastric parietal cells (pernicious anaemia); neurological: MS, MG

55
Q

Systemic autoimmune diseases

A

affect multiple tissues of the body and the Ags recognized are more ubiquitous

56
Q

Examples of systemic autoimmune disease are

A

rheumatoid arthritis, systemic lupus erythematosus (SLE)

57
Q

B cells are involved in which hypersensitivities?

A

II (ligand-mediated reactions) and III (IC deposition)

58
Q

T cells are involved in which hypersensitivities?

A

IV delayed type

59
Q

Loss of central tolerance is linked to defects in which gene?

A

AIRE

60
Q

Loss of peripheral tolerance is linked to defects in which gene?

A

FOXP3 (X-linked) leading to loss of Tregs and peripheral tolerance mechanisms

61
Q

What are examples of B cell mediated autoimmunity?

A

Graves disease (stimulatory Ab; II); Myasthenia Gravis (inhibitory Ab); SLE (III/IC deposition)

62
Q

Examples of T-cell mediated autoimmunity are

A

Type 1 insulin-dependent diabetes mellitus; MS

63
Q

T1 IDDM occurs more frequently in which HLA types?

A

HLA DR3-DQ2 and HLA DR4-DQ8

64
Q

How are T cells implicated in Type 1 IDDM?

A

destruction of pancreatic B cells by T cell reactivity to islet proteins

65
Q

How are the particular MHCs for Type 1 IDDM related to its pathogenesis?

A

thought that these MHCs promote or help present self-antigens more readily

66
Q

How are T cells implicated in MS?

A

T cells specific for myelin antigens promote an inflammatory response that degrades the myelin sheath of nerve axons

67
Q

Which Th cells are predominant in MS destruction?

A

Th1 and Th17 - pro-inflammatory w/IFNy

68
Q

Which Th cells are associated with MS remission?

A

Th2

69
Q

Dysregulation of what cell type is associated with MS?

A

Tregs

70
Q

Which HLA types are more associated with MS?

A

HLA-DR15 and HLA-DQ6

71
Q

What is thought to initiate autoimmune diseases?

A

self-Ags released from injured cells are recognized by B cells; T cells specific for that self peptide activate B cells to differentiate into plasma cells; plasma cells secrete self-Ag Abs that cause inflammation at the injury site, perpetuating the cycle

72
Q

What is the bystander role in autoimmune disease?

A

infection of tissue releases self Ags and infects DCs at the same time; get a B cell with self-Ag reacting with a DC with same Ags; T cell can activate B cell or become self-reactive

73
Q

What is the role of molecular mimicry in autoimmune disease?

A

Ags from a pathogen are similar to those of self-Ags causing cross-reactivity reactions when the immune system is activated of B cells (eg rheumatic fever) and T cells

Microbiology and Immunology (9 decks)

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