3.3.13 Autoimmunity Flashcards

1
Q

Immune Complex disease is type ___. What’s it initiated by & what type of response does it produce?

A

Type III

Initiated by antigen-antibody complexes that can induce an inflammatory response

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2
Q

Describe systemic reaction for type III reaction

A

AG-AB complexes circulate throughout blood stream & settle in certain target organs like kidney initiating an inflammatory response

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3
Q

Major organ in systemic reaction

A

Kidneys

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4
Q

___ can remove immune complexes

A

Neutrophils

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5
Q

Diseases associated w/ immune complex diseases

A

Infectious & postinfectious disease
Autoimmune disease
Drug reactions

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6
Q

Immune complexes that fix complement express ___ which attach to ___ on surface of RBC

A

C3b
CR1

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7
Q

Define kupffer cells

A

(hepatic macrophages) macrophage like cells in liver that remove AG-AB complex from RBC

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8
Q

Site, T cells involved, & time of reaction for cell-mediated delayed hypersensitivity (type IV reaction)

A
  • Site: skin or mucosa
  • T cells involved:
    CD4+ TH1 that release cytokines
  • Time of reaction: 24-72 hours
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9
Q

Examples of type IV reaction

A

tuberculin reaction, contact dermatitis & contact stomatitis

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10
Q

___ is used interchangeably w/ cell mediated immunity

A

Delayed type hypersensitivity

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11
Q

Steps for delayed type hypersensitivity

A
  1. Tuberculin’s introduced subcutaneously (already have effector cells from previous rxn) → processed by APC
  2. TH1 effector cells recognize antigen & releases cytokines
  3. Recruitment of T cells, phagocytes, fluid, & protein to site of antigen injection causes visible lesion
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12
Q

Stimulated TH1 cell causes release of chemokines, cytokines, & cytotoxins. What do each of these result in?

A
  • Chemokines –> macrophage recruitment
  • IFN-gamma –> activates macrophages, increasing release of inflammatory response
  • TNF-alpha & LT –> local tissue destruction, leads to inflammatory response
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13
Q

Contact hypersensitivity 2 phases & steps

A

Sensitization phase
1. Something comes in contact with skin (usually haptens)
2. Haptens are lipid soluble so go into epidermis & interact w/ proteins
3. Langerhans’ cells process the AG-AB complex & take it to lymph node
4. DC interacts w/ naive CD4+ T cell → effector T cell

Elicitation phase
Activation of keratinocytes

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14
Q

What’s significant about haptens?

A

They don’t produce immune response unless they interact w/ protein

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15
Q

Langerhan’s cells vs. DC

A

Langerhan’s process & don’t present
DC present, but DON’T process

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16
Q

Describe patch test

A
  • For contact dermatitis
  • Consists of gauze & gel w/ antigen of interest
  • Held on skin for 24-72 hours
17
Q

___ causes poison ivy reaction. What happens?

A

Pentadecacatechol

  • It penetrates the cell membrane & modified intracellular proteins
  • Modified proteins are broken down & become incorporated into MHC I & are recognized by CD8+
18
Q

Delayed hypersensitivity reaction types & reaction times

A

Contact → 24-72 hours
Tuberculin → 24-72 hours
Granuloma → 21-28 days

19
Q

Granuloma reaction steps

A
  1. IL-12 presented by DC to stimulate naive TH1 cell
  2. Effector CD4+ TH1 produced → releases IFN-gamma & TNF-alpha
  3. Activation of immature macrophage
  4. Macrophage changes in morphology & looks like an epithelial cell
  5. Fusion of epithelioid cells in the presence of tumor necrosis factor (TNF)
  6. Multinucleated giant cell
20
Q

Structure of granuloma

A

Center of it contains multinucleated giant cells & epithelioid cells that are derived from macrophages, which is then surrounded by T cells

21
Q

Define autoimmunity

A

response to self antigens due to lack of tolerance or was never there
- Response may not be harmful

22
Q

Define autoimmune disease

A

loss of tolerance to self antigen that results in immune response that produces a clinical disease
- Produces harmful response

23
Q

What are the 6 mechanisms of self tolerance?

A
  • Negative selection of B cells in BM
  • Expression of tissue-specific proteins in the thymus so that they participate in negative selection of T cells
  • Negative selection of T cells in the thymus
  • Exclusion of lymphocytes from certain peripheral tissues: brain, eye, testis (examples of sequestered antigens)
  • Induction of anergy in autoreactive B & T cells that reach the peripheral circulation
  • Suppression of autoimmune responses by regulatory T cells
24
Q

Example of sequestered antigens?

A

sympathetic ophthalmia

25
Q

Define sequestered antigens

A

antigens that aren’t exposed during development of immune system

26
Q

Treg cell have __ expressed on the surface & ___ transcription factor

A

CD25+
FoxP3

27
Q

Describe central tolerance when autoreactive B cell encounters autoantigen after it leaves BM

A

Autoreactive B cell gets into FDC & sees antigen → no T cell help → B cell destroyed by apoptosis

28
Q

Co-stimulatory signal & specific signal results in

A

Active T cell

29
Q

Specific signal alone (no co-stimulatory signal - missing B7) results in

A

T cell becomes anergic

30
Q

Co-stimulatory signal alone (missing MHC & TCR) results in

A

No effect on T cell

31
Q

5 possible causes of autoimmune diseases

A
  • Cross-reacting antigens (molecular mimicry)
  • Breakdown in lymphocyte regulation
  • microbes
  • environmental
  • genetic
32
Q

Describe cross-reacting antigens

A
  • Antigens shared between humans & microbes
  • Both express same epitope
  • If you make antibody against microorganism, there’s a chance the antibody can react w/ antigens we normally express
33
Q

Example of cross-reacting antigens. What are the steps to develop rheumatic fever?

A

Rheumatic heart disease

Caused by streptococcus (strep throat) → immune response is antibody formation → elimination of streptococcus OR reaction w/ myocardial antigen (can develop rheumatic fever if not treated)

34
Q

Loss of ___ cells can contribute to autoimmune disease

A

Treg

35
Q

Ankylosing spondylitis is associated w/ expression of ___. ___% of patients express it. What’s the relative risk?

A

B27
95%
> 150