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Immunology > Autoimmunity > Flashcards

Autoimmunity Flashcards

1
Q

How do autoimmune diseases come about?

A

Self-Ag is recognized as foreign and there is a failure of regulatory mechanism to control that response

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2
Q

What are the three factors contributing to development of autoimmune diseases?

A

immune factors (breakdown of T or B tolerance), genetic factors, environmental factors

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3
Q

How do these factors contribute to the development of autoimmune disease?

A

Genetic susceptibility means they have genes that allow them to present self-Ag to the immune system, but usually autoimmune response is caused by the response to environmental trigger that is misdirected to self-Ag

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4
Q

How does B cell tolerance break down?

A

not all of self-reactive B cells in BM are deleted, defective B cell anergy (should apoptose but don’t, given T cell help)

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5
Q

How does T cell central tolerance break down?

A

defects in AIRE leads to production of variety of autoimmune B and T cell responses, self-Ag not expressed in thymus

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6
Q

How does T cell peripheral tolerance break down?

A

insufficient control of Tcell costimulation, lower threshold for costimulation activation, variants of CTLA-4 that bind less, variants of CD40/CD40L that allow easier activation

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7
Q

What does a deficiency of FoxP3 mean?

A

lack of regulatory T cells, potential cause of autoimmune disease

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8
Q

What are Th17 cells?

A

helper CD4+ T cells that secrete IL-17

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9
Q

What does IL-17 bind?

A

IL-17 receptors on fibroblasts, epithelial cells, and keratinocytes, leading to secretion of cytokines and recruitment of inflammatory cells

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10
Q

What is the dominant genetic factor affecting susceptibility to autoimmune diseases? What may cause this?

A

HLA, located in MHC region, may be due to role in Ag presentation

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11
Q

What other genes affect susceptibility to autoimmune diseases?

A

complotypes (variants of complements), CTLA-4, AIRE, Fas, FasL, bcl-2, TNF, FoxP3

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12
Q

What are cells with a high level of bcl-2 resistant to?

A

apoptosis

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13
Q

What are sites of immune privilege and how can they be related to autoimmune disorders?

A

Sites of immune privilege are normally isolated from naive lymphocytes so they are not tolerized to these self-Ag, trauma to these sites can release sequestered Ag into circulation and allow attack of self-Ag by effector cells

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14
Q

Why do most autoimmune diseases occur at higher incidence in women?

A

estrogen receptors on T cells, activates T cells in times of estrogen or estrogenic chemical (PCBs and doxins) flare

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15
Q

What is the mechanism of autoimmunity behind celiac disease?

A

self proteins are modified to appear foreign, activates CD4+ T cells

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16
Q

Infection of Group A Strep leads to what?

A

rheumatic fever, carditis, polyarthritis

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17
Q

Infection of chlamydia leads to what? What HLA is associated?

A

Reiter’s syndrome, reactive arthritis, HLA B-27

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18
Q

Infection of shigella, salmonella, yersinia, campylobacter leads to what? What HLA is associated?

A

reactive arthritis, HLA B27

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19
Q

Infection of B. burgdoerferi leads to what?

A

Chronic arthritis in lyme disease

20
Q

Infection of coxsackie, echoviruses or rubella leads to what?

A

Type 1 diabetes

21
Q

How does molecular mimicry instigate an autoimmune repsonse?

A

upon infection, pathogen-derived Ag presented are structurally similar to self-Ag and stimulate a T cell response against self-Ag

22
Q

Infection may lead to increased antigen presentation. How does this occur?

A

IFNgamma induces class II expression on cells that don’t normally act as APCs and increases Class I and Class II expression on APCs

23
Q

What is Hashimoto’s disease?

A

thyroid gland resembles secondary lymphoid tissue with B and T cells present due to induced expression of Class II HLA on thyroid epithelial cells

24
Q

What autoimmune disease type is associated with type II hypersensitivity reaction?

A

antibody-mediated

25
Q

What are 2 examples of ab-mediate autoimmune diseases?

A

autoimmune hemolytic anemia, goodpasture’s syndrome (glomerulonephritis, pulmonary hemorrhage)

26
Q

What is the mechanism of hemolytic anemia?

A

IgG autoAb bind Rh or I antigens and activate complement for either phagocytosis or lysis of RBCs

27
Q

What is the antigen, antibody and consequence of Grave’s disease?

A

ag: thyroid stimulating hormone receptor
ab: agonist of TSH
consequence: hyperthyroidism

28
Q

What is the antigen, antibody and consequence of myasthenia gravis?

A

ag: Ach receptor
ab: antagonist
consequence: progressive muscle weakness

29
Q

What is the antigen, antibody and consequence of insulin-resistant diabetes?

A

ag: insulin receptor
ab: antagonist
consequence: hyperglycemia, ketoacidiosis

30
Q

Why are endocrine glands affected by antibody-mediated autoimmunity?

A

well-vascularized so immune cells can gain access

31
Q

How do anti-Ach receptor Ig cause myasthenia gravis?

A

antiAch receptor Ig binds receptor causing endocytosis and degradation, fewer receptors lead to decreased sensitivity to stimulation and progressive muscle weakening

32
Q

Do IgG-mediated or Tcell-mediated autoimmune diseases present in newborns?

A

IgG-mediated, can be transferred in utero

33
Q

How do you cure a newborn of autoimmune disorder transferred via IgG?

A

plasmapheresis to remove maternal Ab

34
Q

What disease presents with anti-DNA and anti-nucleosome antibodies in immune complexes?

A

SLE

35
Q

Why does the specificity of SLE response broaden over time?

A

the immune complex spreads and deposits elsewhere in body

36
Q

What are 3 examples of T cell-mediated autoimmune diseases?

A

type 1 diabetes, RA, MS

37
Q

What is the antigen in type 1 diabetes?

A

pancreatic b-cell antigen

38
Q

Why is there hyperglycemia in type 1 diabetes?

A

B cells produce little to no insulin due to destruction by inflammatory cytotoxic CD8 T cells

39
Q

What are the antigens of the autoantibodies in RA?

A

constant region of other antibodies (rheumatoid factor)

40
Q

Is rheumatoid factor diagnostic for RA?

A

no, it can be found in other diseases too

41
Q

What causes the joint damage in RA?

A

infiltration of inflammatory CD4 and CD8 cells that produce proteases and collagenases erode structures and damage cartilage

42
Q

What are the antigens of the autoantibodies in MS?

A

myelin basic protein, proteolipid protein, myelin oligodendrocyte glycoprotein

43
Q

How does MS occur?

A

autoimmune response to Ag in the myelin sheath of nerve cells involving Th1 CD4 T cells and macrophages resulting in the production of sclerotic plaques resulting in progressive paralysis

44
Q

What are treatments for autoimmune disorders?

A

physical removal of Ag or immune complex, IV-IgG to remove antibody complex, NSAIDs, deplete immune cells, block activation of immune cells, replacement therapy, hormones

45
Q

What is autoimmune thrombocytopenia?

A

platelet antigens are the targets of autoantibodies

46
Q

What is Goodpasture’s syndrome?

A

IgG against type IV collagen elicits inflammatory response in the renal tissue

47
Q

Describe how SLE induces autoimmune disease.

A

circulating Ab specific for cell surface, cytoplasm, nucleus, nucleic acid, and nucleoproteins produced
autoAb and self-Ag form immune complexes that deposit in blood vessels, kidneys, and joints and initiate inflammatory reactions

Immunology (18 decks)

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