16. Hypersensitivity Reactions (III & IV) Flashcards

1
Q

What causes Type III Hs?

A

large amounts of immune complexes that aren’t removed by normal mechanism

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2
Q

What are some examples of Type III Hypersensitivity disease?

A

Serum sickness, Farmer’s lung caused by inhalation of moldy hay

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3
Q

What are the hallmarks of DTH (Type IV)?

A
  • Delayed time for reaction to develop
    o 1-3 days
  • Purely cell-mediated rather than Ab mediated
  • Recruitment of Macs (as opposed to neutrophils in type III reactions)
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4
Q

Basics of Type IV DTH

A

T helper cells encounter Ag, secrete cytokines that induce localized inflammatory reaction (delayed type hs), cytokines cause large influx of Macs which cause tissue damage

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5
Q

Immune complex =

A

Ab plus soluble Ag

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6
Q

Immune complexes can damage tissue. T or F?

A

TRUE

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7
Q

What type of response occurs if immune complex is deposited near site of Ag entry?

A

localized reaction

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8
Q

(Type III) What type of response occurs if complexes are formed in the blood?

A

reactions develop where deposited

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9
Q

(Type III) After immune complex is formed, what four steps occur:

A
  1. Immune complex activates complement
  2. Generation ofo anaphylatoxins (C3a, C4a, C5a)
  3. Recruit neutrophils and granule release
  4. Anaphylatoxins cause mast cell degranulation
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10
Q

Deposition of immune complexes can trigger

A

release of inflammatory mediators and vasoactive mediators including proteases which may damage connective tissues; clots may form as complexes activate platelets

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11
Q

Deposition of immune complexes in blood vessels causes

A

vasculitis

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12
Q

Deposition of immune complexes in kidneys causes

A

glomerulonephritis

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13
Q

Deposition of immune complexes in joints causes

A

arthritis

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14
Q

Arthus reactions are

A

localized Type III Hs reactions

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15
Q

Why is granuloma a double edged sword?

A

walls off organism in the infected tissue; macrophage lytic enzymes damage the body tissue

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16
Q

Explain skin testing for DTH reactions.

A
  • To determine whether a person has been exposed to M. tuberculosis:
  • PPD (bacterial cell wall protein) is injected intradermally
  • Development of firm, red, swollen lesion @ 48-72 h indicates previous exposure
  • Positive result indicates person has population of sensitized Th1 cells
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17
Q

Skin test for DTH reaction distinguishes whether exposure was to pathogenic for or to vaccination. T or F?

A

FALSE; skin test does not distinguish between exposure to pathogen for or to vaccination

18
Q

Contact dermatitis is a Type IV Hs. T or F?

A

TRUE

19
Q

How can sensitization occur?

A

if a reactive chemical compound binds to skin proteins

20
Q

Type IV Hs can be induced by:

A

pharmaceuticals, cosmetics, industrial chemicals, metal ions, and more

21
Q

What type of Hs can cause strong cell-mediated responses against skin cells, inducing blister-like lesions and rashes?

A

Type IV Hs (DTH)

22
Q

Tolerance =

A

prevention of an immune response against self Ags

23
Q

Central tolerance is the prevention of an immune response against self Ags by what mechanism?

A

deletion of lymphocytes before they mature; central tolerance limits development of autoreactive T and B cells

24
Q

Where does tolerance occur?

A

generative lymphoid organs

25
Q

Peripheral tolerance =

A

either renders self-reactive lymphocytes nonresponsive or actively generates inhibitive lymphocytes outside the bone marrow and thymus

26
Q

Antigen sequestration

A

a means to protect self antigens from attack

27
Q

What are some examples of antigen sequestration?

A

-anterior chamber and lens of eye lack lymphatic drainage
-blood brain barrier
-development of male reproductive cells

28
Q

What does peripheral tolerance regulate?

A

autoreactive cells that made it into circulation

29
Q

Name the 3 steps of peripheral tolerance.

A
  1. if T cells only receive “signal 1” they become anergic
  2. CTLA-4 expression on T cells (in lieu of CD28)
  3. Induction of T regulatory cells
30
Q

T regulatory cells are

A

regulatory CD4+ T cells which can be generated in they thymus or in the periphery following Ag induction

31
Q

Treg cells still engage Ag-MHC Class II complexes through TCR. T or F?

A

TRUE; but they downregulate responses when they do so

32
Q

Name four mechanisms by which Tregs suppress.

A
  1. kill APCs and effector T cells by perforin and granzymes
  2. inhibit APC function via CTLA-4
  3. secrete immune inhibiting cytokines such as IL-10 and TGF-beta
  4. act like a sponge to absorb IL-2 so other T cells can’t get fully
33
Q

Autoimmunity =

A

when the immune system turns on itself due to a lack of self tolerance

34
Q

Some autoimmune diseases are mediated by direct cellular damage. Explain this four step process.

A
  1. lymphocytes or Abs bind to cell-membrane self Ags
  2. cellular lysis and/or inflammatory response
  3. damaged tissue replaced by scar tissue
  4. organ function declines
35
Q

Hashimoto’s thyroiditis is most common in what population?

A

middle aged women

36
Q

Hashimoto’s thyroiditis decreases the function of what?

A

thyroid function, leading to hypothyroidism

37
Q

Explain the role of Ab in Hashimoto’s thyroiditis.

A

Auto Abs and Th1 cells produced are specific for thyroid Ags; Ab produced interferes with iodine uptake

38
Q

Diseases characterized by induced DTH response in the thyroid.

A

Hashimoto’s Thyroiditis

39
Q

Goiter

A

visual enlargement of the thyroid gland as a result of inflammation induced by DTH response in thyroid (intense WBC infiltration)

40
Q

CTLA-4 expression only occurs on what type of cells?

A

activated T cells

41
Q

CTLA-4 binding to _________________ inhibits T cells.

A

CD80/86

42
Q

Mice lacking CTLA-4 show widespread _________________ disease.

A

autoimmune