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Immunology 2 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

describe type 1 hypersensitivity

A

allergic reactions. IgE is created in response to a innocuous antigen. they attach to Fc receptors on mast cells and are ready to react with a subsequent exposure.

mast cells produce degranulation (histamine), eosinophil, neutrophil, lymphocyte, and macrophage recruitment, smooth muscle contraction, and increased vascular permeability.

reactions only occur after prior sensitization but occur immediately after secondary exposure.

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2
Q

what are the 4 ways you can come into contact with an allergen?

A
  1. injestion
  2. inhalation
  3. contact
  4. injection
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3
Q

what are some systemic symptoms seen with type 1 hypersensitivity

A

skin: pruritis (itching), edema (swelling), urticaria (hives)
pulmonary: bronchospasms, mucosal edema w/ airway obstruction, laryngeal edema
CV: hypotension, arrhythmias,
GI: cramps, vomiting, diarrhea

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4
Q

what are the Fc receptors on mast cells that bind IgE

A

Fc3RI

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5
Q

what is the difference between mast cells and basophils

A

both respond to IgE, but mast cells are found in the connective tissue and mucosa near blood vessels whereas basophils circulate

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6
Q

how are mast cells activated?

A

cross-linking of bound IgE

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7
Q

describe the effects of histamine

A

H1 receptor: contracts smooth muscle, increases vascular permeability, increases mucous secretion

H2 receptor: increases gastric secretion, decreases mediator release by basophils/mast cells

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8
Q

describe the effects of prostaglandin D

A

vasodilation and edema, bronchoconstriction, muscus secretion, itching

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9
Q

describe the effects of SRS-A (LTC, LTD, LTE)

A

derived from arachidonic acid, bronchoconstrictors, increased dilation and permeability of microvessls, edema, coronary and cerebral vasoconstriction, increased mucous, decreased contractility, and increased gastric acidity

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10
Q

describe the effects of leukotriene B

A

neutrophil, macrophage, and eosinphil attractant, edema (increased permeability)

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11
Q

describe the effects of platelet activating factor

A

vasodialator, bronchoconstrictor, increased permeability, chemotaxis and degranulation

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12
Q

describe the effects of proteases

A

activate kinins, complement, and endothelial cells which increase permeability, decrease BP, vasoconstriction

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13
Q

what are anaphhylatoxins

A

C3a, 4a, 5a- chemoattractants of the complement system that also cause vasoconstriction

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14
Q

what mediators can cause tissue destruction?

A

toxic oxygen radicals (from phagocytes) and acid hydrolases and neutral proteases (mast cell granules)

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15
Q

/what are some non-immunological mechanisms that can lead to anaphylaxis?

A

NSAIDs
cold
exercise

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16
Q

how can drugs be used to treat type 1 rxns

A

inhibit mediator action:
histamine antagonists: sneezing, runny nose, itchy eyes
leukotriene antagonists: asthma, anaphylaxis
steroids
epinephrine- low bp, brochospasm

inhibit mediator production
glucocorticoids
IgE antibodies
leukotriene synthesis inhibitors

17
Q

subcutaneous immunotherapy

A

hyposensitization- slowly increasing the dose of subQ allergen injection. allergen specific t-regs are activated, increasing levels of IgG and IgA for allergen removal, which does not use mediators like the IgE.

18
Q

describe type 2 hypersensitivity reactions

A

IgG or IgM bind to host cells, causing destruction via complement or cytolytic cells

19
Q

how are ABO blood types different?

A

a different terminal sugar residue on the backbone of a glycoprotein

20
Q 
describe the following type 2 conditions:
transfusion reaction
hemolytic disease of the newborn
autoimmune blood dyscrasias
hyperacute graft rejection
transfusion related acute lung injury
A

transfusion reaction: recipient reacts against foriegn donor blood sugars

hemolytic diease of the newborn- newborn has RhD+ and mom is -. during first birth mom is exposed to D+, placing second child at risk if they are also D+

dyscrasias- autoantibodies recognize ones own blood cells

graft- hyperacute rejection occurs when a recipient is already sensitized to antigens found in the donor. this only occurs in grafts that are revascularized directly during transplantation (kidney)

TRALI- abs in donated plasma induce serious rxns

21
Q

what are the treatment options for type 2 rxns?

A 
transfusion
plasma exchange
glucocorticoids
cytotoxic drugs/anti-b cell drugs
splenectomy
IVIG
drugs to stimulate RBC/platelet production
22
Q

what is type 3 hypersensitivity?

A

the destructive inflammatory lesions that result from tissue deposition of complexes w/ antigen, ab, and complement

23
Q

serum sickness

A

animal serum was injected into humans and caused a type 3 rxn. human abs specific to animal abs form and result in the deposition of ab complexes in the tissue, causing damage by the mediator release and inflammation.

symptoms clear in acute cases (ie serum sickness) but chronic cases occur when the offensive ag is persistent (ie autoags, viruses).

24
Q

type 3 diseases are often identified by the site at which they occur: lymphadenitis, necrotising vasculitis, periarteritis nodosa, and arthritis

A

ok

25
Q

how do soluble complexes form?

A

they form when there is a moderate excess of ag (3ag/2ab). the size of the complex is an important determinant of its potential to do damage. some are the optimal size to escape phagocytosis but get stuck in blood vessels or between epithelia

26
Q

what happens to an immune complex when it is recognized?

A

IgG crosslinks with Fc receptors on neutrophils to produce leukotriene B4 and IL8, activating macrophages neutrophils and mast cells to produce leukotrienes C D and E. combined, these mediators cause increased vascular permeablity, which facilitates the movement of immune complexes to the basement membrane.

simultaneously, complement is also activated by IgG and C3a and 5a act as chemoattractants for neutro and eosinophils

27
Q

arthus rxn

A

Ab is in gross excess and injected intradermally. forms a complex that precipitates within venules w/in 3-8 hours

28
Q

how are complexes cleared?

A
  1. macrophages- via Fc receptors and C3b
  2. erythrocytes- contain C3b receptors- bind to and carry complexes to the liver, where kupffer cells remove them
  3. complement- alternate complement pathway facilitates destruction
  4. neutrophils
  5. any other cells with Fc or C3 receptors
29
Q

what factors are important in determining the behavior of the complex?

A
  1. ab isotype
  2. ag
  3. complex size
  4. ab/ag ratio
  5. ability to fix complement
  6. concentration of complex
30
Q

what assays can be used to detect immune complexes?

A
  1. C1q- C1q binds the complex and then can be detected w/ a labeled ab
  2. CH50- measure serum complement levels. activated complement will decrease the amount of soluble complement in the serum
  3. immunohistology
31
Q

what are the treatment options for type 3 hypersensitivity

A
  1. withdraw culprit ag
  2. symptomatic- antihistamines, NSAIDS
  3. glucocortidoids- for more severe cases
32
Q

what is type 4 hypersensitivity

A

delayed type hypersensitivity- t-cell mediated

results from the reintroduction of an antigen that activates t-cell immunity. the DTH response results from the inflammatory mediators from th1 and th17 t cells or CTLs.

major causes= autoimmunity (usually limited to one tissue; not systemic) and persistent responses to environmental antigens

33
Q

tuberculosis causes type 4 sensitivity and it is the basis of the PPD test

A

ok

34
Q

compare the onset, duration, ab class, ab quantity, primary mediators, key cells, and transfer mechanisms of type 1, 2/3, and 4 hypersensitivities

A

type 1- immediate onset, 1 hr duration, IgE ab, .01 ug quantity, mast cells factor mediators, mast cells, and can be transfered with serum or cells

type 2- 2 hr delayed onset, 24 hr duration, IgD or IgM ab, 100 ug quantity, PMN mediators, transfered with serum or cells

type 4- 15 hr onset, 5 day duration, no abs involved, t-cell mediated, only transfered with cells

35
Q

describe the 4 subtypes of type 4 sensitivity

A

4a- th1 mediated, IFN-y and TNF-a driven, macrophage effectors

4b- th2 mediated, IL-4, 5, 13 driven, eosinophilic inflammation

4c- CTL mediated, perforin/ granzyme/ FasL driven, CD8 killing

4d- T cell mediated, CXCL-8/GMCSF driven, t cells recruit PMNs

36
Q

tuberculin type hypersensitivity

A

the mantoux rxn is DTH rxn to tuberculin. after 12-24 hours, erythema and induration develop at the site on inoculation in pts previously exposed via TB infection or BCG vaccination

37
Q

contact hypersensitivity

A

small molecules (haptens) interact with self proteins and are taken up by DCs, stimulating t-cells. upon reintroduction of the antigen (posion ivy, certain metals) a t-cell mediated response occurs

response is primarily driven by CD4, although CD8 does contribute

38
Q

granulomatous hypersensitivity

A

d/t persistent antigen presence, often because they are difficult to remove

Immunology 2 (6 decks)

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