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Immunology > CH. 16 Autoimmune Diseases > Flashcards

CH. 16 Autoimmune Diseases Flashcards

1
Q

What is central tolerance?

A

-deletion of lymphocytes in primary lymphoid organs before they mature; limits development of autoreactive T- and B-cells

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2
Q

During central tolerance, B cells have been shown to undergo

A

receptor editing

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3
Q

Peripheral tolerance

A

either renders self-reactive lymphocytes nonresponsive (anergic) or actively generates inhibiting lymphocytes outside the BM and thymus; regulates autoreactive cells in circulation

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4
Q

Dependent mechanisms of CD4+ T cells

A
  • occur as TREG cells express high levels of inhibitory CTLA-4 molecules
  • CTLA-4 blocks CD28 activation through CD80/86, inhibiting APC activation/licensing
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5
Q

Independent mechanisms of CD4+ T cells

A

rely upon secretion of cytokines (IL-10, TGF-B, IL-35) into the surrounding area, shutting down nearby cell responses
-these mechanisms halt costimulation and activate indoleamine 2,3-dioxygenase, responsible for cleaving tryptophan, creates kynurenines, which inhibits T cells

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6
Q

In what ways do CD4+ T cells maintain tolerance?

A

work via contact dependent and independent mechanisms

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7
Q

What current mechanisms are anticipated to allow regulatory CD8+ T cells to maintain tolerance?

A
  • not likely generated in the thymus, but instead in the periphery during CD8+ T-cell activation induction events (appear after Ag-MHC class I stimulation in the presence of TGF-B)
  • Most likely use a range of mechanisms to suppress activity (lysis of APCs, inhibition of APC function, regulation of effector cells that bind the same Ag)
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8
Q

What factors can predispose an individual for tolerance rather than stimulation?

A
  • high doses of antigen
  • long-term persistence of antigen in the host
  • intravenous or oral introduction
  • absence of adjuvants
  • low levels of costimulation
  • presentation of antigen by immature or unactivated APCs
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9
Q

What percentage of people in industrialized countries are estimated to have an autoimmune disease?

A

3-8%

  • caused by failure of tolerance processes
  • may be organ-specific or systemic
  • may involve antibodies, T cells, immune complexes, or any combination of elements
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10
Q

What factors predispose an individual for developing an autoimmune disease?

A
  • studies have linked sex hormones to gene expression changes that could help explain why women experience autoimmune diseases more frequently
  • intrinsic and extrinsic factors can favor susceptibility to autoimmune disease
  • The roles of genes in susceptibility to autoimmunity (certain MHC genes linked to specific autoimmune disorders)
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11
Q

In most organ-specific autoimmunities, what four areas are treatments aimed at?

A
  • increasing levels of missing, required gene products (thyroid hormone, insulin, acetylcholine)
  • decreasing antibody production (B cell inhibitors)
  • decreasing inflammatory mediators (TNA, IL inhibitors)
  • decreasing costimulatory signals (CD80/86 inhibitors)
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12
Q

What potential side effects are affiliated with long-term use?

A
  • general toxicity, often to rapidly dividing cells (hair follicles, intestinal lining, blood cells)
  • also predisposes individuals to uncontrolled infections
  • can promote development of cancer by removing anti-tumor T and NK cells
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13
Q

What is the holy grail of immunotherapy in treating autoimmunity?

A

Antigen-specific immunotherapy

stimulate tolerance to the auto-Ag, restoring balance

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14
Q

What is an example of the holy grail of immunotherapy in treating autoimmunity?

A

glatiramer acetate has been used to treat MS

  • four basic AAs found in mylein basic protein
  • selectively increases TREG cells, modulating APC function
  • although shifts T cell populations, it has shown only modest improvement over standard therapies
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15
Q

What are the four types of tissue transplantations?

A
  • autograft
  • isograft
  • allograft
  • xenograft
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16
Q

Autograft

A

transplant from the same individual

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17
Q

Isograft

A

tissue transplant from genetically identical sibling or clone

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18
Q

Allograft

A

transplant from genetically different member of the same species

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19
Q

Xenograft

A

transplant from different species

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20
Q

First-set rejection

A

complete by 12-14 days, but memory of the anti-graft response is generated; first exposure

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21
Q

Second-set rejection

A

occurs much faster, completing within only 5-6 days; secondary immune iresponse

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22
Q

What is the role of T cells in graft rejection

A

T cells mediate graft rejection

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23
Q

Which type of T cells facilitate rejection?

A

-CD4+ more important, but CD8+ does too

24
Q

Histocompatible

A

tissues that are antigenically similar

25
Q

How do you determine MHC compatibility?

A

Cross-matching

26
Q

What allows organ transplant between completely mismatched people?

A

anti-rejection drugs (immunosuppressants)

27
Q

Sensitization Stage of Graft Rejection

A

CD4 and CD8 cells recognize alloantigens expressed on foreign graft cells

  • T cells proliferate in response
  • May recognize donor MHC molecules directly
  • may recognize peptides from donor MHCs presented in the recipient’s own APC MHC molecules (indirect)
  • Memory T cells generated
28
Q

Effector Stage of Graft Rejection

A
  • generally involves heavy infiltration of recipient cells into graft tissue (similar to DTH reaction)
  • can rarely involve production of Abs against donor HLA molecules or endothelial Ag
29
Q

Hyperacute rejection

A
  • by preexisting antibodies
  • occurs before grafted tissue ever revascularizes
  • antibodies bind to graft cells and activate complement
  • complete rejection may occur in as few as 24 hours
30
Q

Acute rejection

A
  • mediated by T-cell responses
  • begin 7-10 days post-transplantation
  • induce massive infiltration of lymphocytes and macrophages
  • rejection occurs through mechanisms described for effector stage of graft rejection
31
Q

Chronic rejection

A
  • develops months or years after acute rejection reactions have subsided
  • mechanisms include humoral and cell-mediated recipient responses
  • anti-rejection drugs help, but are not perfect
32
Q

Total lymphoid irradiation

A

-used to eliminate lymphocytes
-lymphocytes extremely sensitive to x-rays
often used in bone marrow transplants or to treat GvHD
-repeated x-ray exposures to the thymus, spleen, and lymph nodes
-effectively wipes out the recipient’s own immune cells, creating a situation where donor stem cells can engraft and form a “new” immune system safely

33
Q

Azathioprine

A
  • mitotic inhibitor that diminishes B- and T-cell proliferation
  • can dramatically increase survival rates of allografts by inhibiting proliferation of these cells
  • often prescribed with corticosteroids to prevent inflammation
34
Q

Cyclophosphamide

A

inserts into DNA helix, disrupting it

35
Q

Cyclosporin A (CsA)

A
  • fungal metabolite
  • acts to decrease synthesis of inflammatory cytokines by preventing the activation of key transcription factors
  • not without side effects, including kidney toxicity
36
Q

In Hashimoto’s Thyroiditis, what is produced?

A

autoantibodies and sensitized TH1 cells specific for thyroid antigen

37
Q

What do autoantibodies produced in Hashimoto’s Thyroiditis do?

A

interfere with iodine uptake by thyroid, which decreases production of thyroid hormone. This results in hypothyroidism

38
Q

In Hashimoto’s Thyroiditis, a delayed-type hypersensitivity reaction occurs which results in:

A

inflammation –> goiter

39
Q

Functions of thyroid hormone

A
  • controls basal metabolic rate
  • protein synthesis
  • sensitivity to other hormones
40
Q

What causes Type 1 Diabetes?

A

autoimmune attack against insulin-producing Beta cells in the pancreas

41
Q

Type 1 Diabetes: After CTLs infiltrate the pancreas and activate macrophages, what happens?

A

Followed by cytokine release and production of autoantibodies, which may activate complement or antibody-dependent cell-mediated toxicity activities by NK cells

42
Q

In Myasthenia Gravis, what do autoantibodies do?

A

bind acetylcholiine receptors on motor end plates of muscles

43
Q

In Myasthenia Gravis, the binding of autoantibodies on acetylcholine receptors induces:

A

complement-mediated lysis of cells

44
Q

In SLE, what kinds of autoantibodies are produced?

A

autoantibodies against DNA, histones, platelets, and other self structures

45
Q

symptoms of SLE

A
  • fever
  • weakness
  • kidney dysfunction
  • frequent skin rashes
46
Q

in SLE, autoantibodies against RBCs and platelets induce

A

complement-mediated lysis

47
Q

In SLE, autoantibodies against nuclear antibodies can deposit on walls of small blood vessels resulting in:

A

type III hypersensitivity reaction

48
Q

In MS, autoreactive T cells form:

A

inflammatory lesions along myelin sheaths around nerve fibers in the brain and spinal cord

49
Q

Breakdown of myelin sheaths around nerves leads to a range of symptoms:

A

numbness to paralysis and loss of vision

50
Q

What virus may predispose a person to MS?

A

Epstein-Barr virus

51
Q

What factors may predispose a person to MS?

A
  • Epstein-Barr virus
  • hygiene hypothesis
  • sunlight exposure
52
Q

_______ is a known immune modulator that promotes anti-nflammatory response.

A

Vitamin D

53
Q

What is the major symptom of Rheumatorid arthritis?

A

chronic inflammation in joints

54
Q

In rheumatoid arthritis, autoantibodies are reactive with:

A

determinants in the Fc region of IgG

55
Q

Rehumatoid factos are often produced in rheumatoid arthritis and form _____ complexes and activate complement cascades.

A

immune

Immunology (17 decks)

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