16. Hypersensitivity Reactions (III & IV) Flashcards

(42 cards)

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?

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
Peripheral tolerance =
either renders self-reactive lymphocytes nonresponsive or actively generates inhibitive lymphocytes outside the bone marrow and thymus
26
Antigen sequestration
a means to protect self antigens from attack
27
What are some examples of antigen sequestration?
-anterior chamber and lens of eye lack lymphatic drainage -blood brain barrier -development of male reproductive cells
28
What does peripheral tolerance regulate?
autoreactive cells that made it into circulation
29
Name the 3 steps of peripheral tolerance.
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
T regulatory cells are
regulatory CD4+ T cells which can be generated in they thymus or in the periphery following Ag induction
31
Treg cells still engage Ag-MHC Class II complexes through TCR. T or F?
TRUE; but they downregulate responses when they do so
32
Name four mechanisms by which Tregs suppress.
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
Autoimmunity =
when the immune system turns on itself due to a lack of self tolerance
34
Some autoimmune diseases are mediated by direct cellular damage. Explain this four step process.
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
Hashimoto's thyroiditis is most common in what population?
middle aged women
36
Hashimoto's thyroiditis decreases the function of what?
thyroid function, leading to hypothyroidism
37
Explain the role of Ab in Hashimoto's thyroiditis.
Auto Abs and Th1 cells produced are specific for thyroid Ags; Ab produced interferes with iodine uptake
38
Diseases characterized by induced DTH response in the thyroid.
Hashimoto's Thyroiditis
39
Goiter
visual enlargement of the thyroid gland as a result of inflammation induced by DTH response in thyroid (intense WBC infiltration)
40
CTLA-4 expression only occurs on what type of cells?
activated T cells
41
CTLA-4 binding to _________________ inhibits T cells.
CD80/86
42
Mice lacking CTLA-4 show widespread _________________ disease.
autoimmune