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MSS-IHL Final Exam > Tolerance and Autoimmunity > Flashcards

Tolerance and Autoimmunity Flashcards

1
Q

tolerance

A

unresponsiveness to self antigens

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2
Q

autoimmunity

A

results when immune system recognizes self antigens

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3
Q

anergy

A

functional unresponsiveness

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4
Q

central tolerance

A

takes place in central lymph organs

  • B cells in bone marrow
  • T cells in thymus

ex/ negative selection

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5
Q

peripheral tolerance

A

what mature lymphocytes undergo out in body
-lymph nodes and spleen

ex/ T reg function, anergy, cell death

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6
Q

T cell development?

A

positive and negative selection

ones that recognize MHC - selected for

central tolerance

negative selection if high affinity for MHC and self-antigens

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7
Q

Foxp3

A

transcription factor

signals to become a T reg cell

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8
Q

where are T reg cells formed?

A

thymus

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9
Q

when does selection for T reg cells occur?

A

intermediate affinity

-upregulate Foxp3

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10
Q

function of T reg cell

A

check on immune system to keep it from going out of control

also involved transplantation tolerance

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11
Q

peripheral T cell tolerance?

A

Regulatory T cells in the periphery

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12
Q

what do T reg cells express?

A

Foxp3 and CD25

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13
Q

CD25

A

on T reg cells

is the IL-2 receptor

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14
Q

what do T reg cells secrete?

A

IL-10 and TGF-beta

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15
Q

T reg cells depend on what for survival?

A

IL-2

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16
Q

T reg cells?

A

CD4+

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17
Q

anergy?

A

peripheral T cell tolerance

-occurs when T cells activated without co-stimulation**

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18
Q

what happens without co-stimulation in T cell activation?

A

leads to signaling block

-leads to anergy of T cell

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19
Q

what can lead to anergic T cell?

A

1 signal without co-stimulation

2 engagement of inhibitory receptors (CTLA-4)

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20
Q

co-stimulation in T cells?

A

B7:CD28 interaction

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21
Q

what could break anergy?

A

a very strong danger signal

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22
Q

cell death in T cells?

A

peripheral tolerance

  • normally anti-apoptotic signals are higher
  • absence of co-stimulation has more pro-apoptotic signals
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23
Q

Fas and FasL?

A

upregulated when T cell recognizes self antigen

results in apoptosis

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24
Q

what can mutations in Fas result in?

A

children with autoimmune diseases

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25
Q

tolerogenic antigens?

A

usually in generative organs
high concentrations

long-lived exposure (bc its self)

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26
Q

immunogenic antigens?

A

in blood and periphery

short lived

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27
Q

central B cell tolerance?

A

in bone marrow
if recognizes self antigen (T-independent antigen)
-can die (apoptosis)
-can undergo receptor editing

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28
Q

peripheral B cell tolerance

A

anergic
-if self antigen recognition without T cell help

apoptosis
-exclusion from the lymphoid follicle

29
Q

immature B lymphocyte?

A

IgM+ and IgD-

30
Q

tolerance-sensitive cell for T cells?

A

CD4+ CD8+ (double positive) T cells

31
Q

effector mechanisms of autoimmunity?

A

circulating autoantibodies and autoreactive T lymphocytes

32
Q

principle factors in development of autoimmunity?

A

susceptibility genes and environmental triggers

33
Q

Type I diabetes

A

autoimmune destruction of beta cells in pancreas

  • genetic predisposition - Dq8
  • thought to be an environmental trigger

can predict the onset based on autoantibodies

goes through phases:

  • genetic predisposition
  • insulitis
  • pre-diabetes (loss of first phase insulin response)
  • diabetes
34
Q

insulitis

A

beta cell death (type I diabetes)

35
Q

types of autoimmune disease?

A

organ-specific and systemic

36
Q

what sex has more autoimmune diseases?

A

female

  • much more likely in women
  • don’t know why
37
Q

factors contributing to autoimmunity

A

genes, infections, and environmental factors

38
Q

HLA-B27

A

ankylosing spondylitis

autoimmune disorder

39
Q

HLA-DR4

A

rheumatoid arthritis

autoimmune disorder

40
Q

HLA-DR3/DR4

A

Type I diabetes mellitus

41
Q

HLA-DR4

A

pemphigus vulgaris

autoimmune disorder

42
Q

AIRE

A

gene that if we lose will result in autoimmune polyendocrine syndrome (APS-1)

responsible for expressing self antigens in the thymus (no negative selection)

43
Q

Foxp3

A

defects in this gene lead to deficiency of regulatory T cells

can lead to X-linked polyendocrinopathy and enteropathy (IPEX)

44
Q

Fas

A

defect leads to autoimmune hypoproliferative syndrome (ALPS)

defective apoptosis of self-reactive T and B cells in periphery

45
Q

IPEX

A

from loss of Foxp3 gene

46
Q

what would cue you to think a single gene defect?

A

multiple autoimmune disease at early age

47
Q

action of IL-10

A

suppress IgE production

48
Q

action of TGF-beta

A

inhibit IgE prduction

49
Q

what do T reg cells secrete?

A

IL-10 and TGF-beta

50
Q

how does IL-4 and IL-13 induce IgE formation?

A

activate STAT6 to induce isotype switching

51
Q

how does TGF-beta induce IgE formation?

A

inhibit Id2-repressor of IgE isotype switching

52
Q

treatment of IPEX

A

bone marrow transplant
-to restore Foxp3 expressing cells

poor prognosis for IPEX

53
Q

triggers of autoimmunity?

A

presence of microbe induces co-stimulators on the APC presenting self antigen

molecular mimicry - microbe antigen resembles the self tissue

54
Q

streptococcus pyogenes?

A

rheumatic fever

molecular mimicry for protein on heart muscle

activated T cells will attack cardiac muscle

55
Q

what is pathogenic in lupus?

A

antibody

56
Q

what is pathogenic in diabetes?

A

T cells

57
Q

what is pathogenic in myasthenia gravis?

A

antibody

58
Q

what is pathogenic in multiple sclerosis?

A

T cells

59
Q

autoantibodies

A

can be stimulatory or blocking

60
Q

stimulatory autoantibodies?

A

ex/ bind the TSH receptor and result in upregulation of thyroid hormones

Graves disease

61
Q

inhibitory autoantibodies?

A

ex/ bind the acetylcholine receptor (without activation)
-prevent the muscle activity

myasthenia gravis

62
Q

effect of corticosteroids?

A

immunosuppression

63
Q

cyclophosphamide

A

immunosuppression

64
Q

multiple sclerosis

A

Th1 cell response against mylein

more likely in women HLA-DR2

65
Q

oligoclonal immunoglobulins in central nervous system for MS?

A

never been exposed to all these new self antigens!

66
Q

treatment of multiple sclerosis?

A

corticosteroid, cyclophosphamide, IFN-beta

67
Q

treatment of MS with IFN-gamma not favorable?

A

because promoting Th1 cytokines (don’t want that)

68
Q

why feed MBP (myelin basic protein) to mice to prevent EAE?

A

because this would place self-antigen in their bodies (induce peripheral tolerance)

69
Q

can you induce EAE in CD28 knockout mice?

A

no because no co-stimulation

CTLA-4 mice would be really terrible EAE

MSS-IHL Final Exam (15 decks)

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