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MAD Exam 3 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

ACID Acronym for Hypersensitivity Rxns

A

Type I = Anaphylactic and Atopic
Type II = Cytotoxic (antibody-mediated)
Type III = Immune Complex
Type IV = Delayed (T-cell mediated)

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2
Q

type I hypersensitivity is mediated by what class of immunoglobulin

A

IgE

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3
Q

examples of type I hypersensitivity reactions

A
  1. systemic anaphylaxis
  2. acute urticaria (hives)
  3. allergic rhinitis (hay fever)
  4. asthma
  5. food allergies
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4
Q

systemic anaphylaxis response

A

-edema
-increased vascular permeability
-tracheal occlusion
-circulatory collapse
-death

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5
Q

steps of type I hypersensitivity reactions

A
  1. initial allergen exposure (sensitization)
  2. IgE production (as a result of IL-4 and IL-13) by plasma cells
  3. IgE binds to mast cells
  4. allergen cross-link IgE on mast cells
  5. mast cells release mediators (DEGRANULATE) on 2nd exposure [release of histamine, PGE, LT, PAF, and cytokines]
  6. early phase effects and promotion of late phase effects
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6
Q

where does IgE bind to mast cells

A

Fc epsilon receptor
*occurs after INITIAL exposure to the allergen

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7
Q

what happens on FIRST exposure to an allergen in a type I HSR

A

IgE is produced, and the IgE attaches to the Fc epsilon receptor on mast cells

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8
Q

what happens on SECOND exposure to an allergen in type I HSR

A

*the allergen binds and cross-links the IgE on the mast cell surface
*this causes degranulation of mast cells, releasing cytokines and second messengers

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9
Q

degranulation is caused when ?

A

an antigen cross-links IgE on the cell surface

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10
Q

what cytokines induce class-switching to IgE during type I HSR

A

IL-4 and IL-13

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11
Q

source of IL-4 for IgE class switching in type I HSR

A

*derived initially from NK1.1 T cells
*subsequently derived by activated Th2 cells and mast cells

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12
Q

source of IL-13 for IgE class switching in type I HSR

A

produced by Th2 cells and mast cells

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13
Q

important cytokines released by mast cells

A

IL-3, IL-5, and GM-CSF
*promote eosinophil production and activation

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14
Q

IL-5 effects upon release from mast cells during type I HSR

A

*stimulates the production of EOSINOPHILS in the bone marrow
*promotes EOSINOPHIL ACTIVATION
*can help with diagnosis

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15
Q

eosinophil cationic protein

A

*toxic to parasites
*neurotoxin

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16
Q

atopy

A

*condition exhibited by allergic individuals
*atopic individuals exhibit higher than normal levels of circulating IgE and eosinophils
*linked to several genetic loci, including CYTOKINE GENES and HLA CLASS II ALLELES

17
Q

early phase effects of degranulation in type I HSRs

A

*depends on WHERE you have these cells
1. GI tract: expulsion of GI contents (diarrhea and vomiting)
2. airways: congestion and blockage of airways; swelling and mucus secretion in nasal passages
3. blood vessels: increased fluid in tissues, etc

18
Q

immediate (early) phase response in type I HSRs

A

*production of prostaglandins, leukotrienes, platelet activating factors, histamine, TNF alpha, and IL-5 results in RECRUITMENT AND ACTIVATION OF Th2 CELLS, EOSINOPHILS, BASOPHILS, and NEUTROPHILS

19
Q

late phase response in type I HSRs

A

*occurs 8-12 hours AFTER immediate response
*mast cells and basophils release cytokines that PROMOTE cellular INFLAMMATION

20
Q

treatment of asthma (a type I HSR)

A
  1. reducing the effects of inflammatory modulators (inhaled corticosteroids or beta-2 agonists)
  2. reduce antigen intolerance (allergy shots to introduce increased doses of allergen)
  3. monoclonal antibodies (anti-IgE mab, anti-IL-4 mab, anti-TNF alpha mab)
21
Q

normal flora, Tregs, and type I HSRs

A

*hypothesis that the changes in microflora over the past few decades, induced by increased use of antibiotics, has lead to an increase in incidence of allergic diseases
*normal microbiota may promote ACTIVATION OF Tregs in the GI tract

22
Q

regulatory T cells

A

*CD4+, CD25+, FOXP3+ T cells
*arise in the thymus
*activated by dendritic cells
*function to SUPPRESS THE IMMUNE SYSTEM by releasing TGF-beta and IL-10 (inhibit CD4 and CD8 effector functions)

23
Q

syndrome associated with FOXP3 deficiency

A

IPEX syndrome
*due to lacking Tregs

24
Q

type II HSRs - overview

A

antibodies bind to cell surface antigens and cause:
1. cellular destruction: cell is opsonized, leading to phagocytosis, complement activation, and/or NK cell killing
2. inflammation - binding of antibodies causes complement activation and Fc-mediated inflammation
3. cellular dysfunction - antibodies bind to cellular receptors, leading to abnormal blockades or activation of downstream processes

25
Q

NK cell killing in type II HSRs

A

*IgG produced against self-antigen and binds the cell
*IgG also binds to Fc receptor on NK cell
*NK cell releases PERFORINS and GRANZYMES, leading to cell destruction

26
Q

hemolytic anemia of a newborn (a type II HSR)

A

*Rh NEGATIVE MOM carries Rh-positive fetus
*during first delivery, fetal RBCs enter maternal circulation, resulting in SENSITIZATION (mom makes antibodies against baby’s Rh)
*in a subsequent pregnancy, anti-Rh antibodies (IgG) cross the placenta, resulting fetal damage/death

27
Q

prevention of hemolytic anemia of newborn

A

give mom anti-Rh IgG (Rhogam) at time of first delivery; prevents mom from making her OWN antibody against Rh

28
Q

type III HSRs - components

A

IMMUNE COMPLEX:
1. antigen and antibody (IgG) interact and activate complement
2. complement activation attracts neutrophils
3. neutrophils release lysosomal enzymes, which cause cellular damage

29
Q

type III HSRs - locations

A
  1. if complexes are retained locally, then the damage is also local (arthus reaction)
  2. if immune complexes can circulate, then systemic, multi-organ effects occur (glomerulonephritis)
30
Q

arthus reaction (type III HSR)

A

a local, IMMEDIATE type III HSR at the site of injection
*results in local inflammation, edema and/or necrosis

31
Q

serum sickness (type III HSR)

A

DELAYED type III HSR due to antibodies against foreign proteins:
1. antibodies are produced against proteins in the week following an injection/infusion
2. eventually, immune complexes deposit in membranes throughout the body, where they fix complement
3. RESULT = systemic symptoms appearing 5-10 days post-infusion: fever, urticaria, arthralgia, proteinuria, and lymphadenopathy

32
Q

type IV HSRs - 2 types:

A
  1. direct T-cell cytotoxicity (CD8 cells)
  2. delayed-type hypersensitivity (CD4 cells)
    *BOTH generally occur 24-72 hours after antigen exposure
33
Q

type IV HSR - direct T-cell cytotoxicity

A

*CD8 + T cells DIRECTLY KILL targeted cells

34
Q

type IV HSR - delayed-type hypersensitivity

A

*sensitized CD4+ T cells encounter antigen and release cytokines; resulting inflammation and activation of macrophages results in death of targeted cells

35
Q

type IV HSR - the 4 Ts

A
  1. T-cells
  2. transplant rejections
  3. TB skin tests
  4. touching (contact dermatitis)
36
Q

type IV HSRs - examples

A

*type I diabetes
*TB skin test
*contact dermatitis (poison ivy)
*graft-versus-host disease

37
Q

selective IgA deficiency

A

*most common primary immunodeficiency
*most patients are asymptomatic
*can present with AIRWAY infections, ATOPY, AUTOIMMUNE DISEASE, and ANAPHYLAXIS to IgA-containing products
*susceptible to Giardiasis in particular

MAD Exam 3 (28 decks)

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