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CMBM Exam 4 > Type I, II and III Hypersensitivity > Flashcards

Type I, II and III Hypersensitivity Flashcards

1
Q

Four types of hypersensitivity reactions chart

A
  • Types II, III, IV are directed against self-tissue
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2
Q

Type I hypersensitivity reaction definition

A
  • Rapid immunologic reaction occuring within minutes after a combination of an antigen w/antibody bound to mast cells in individuals previously sensitized to the antigen
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3
Q

Properties of antigens

A
  • Proteins or chemical bound to proteins
  • Chronic exposure
  • Do not stimulate the innate immune system
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4
Q

Common causes of hypersensitivity reactions

A
  • Inhaled materials

*pollens, dander, mold, feces

  • Injected materials

*venoms, vaccines, drugs, therapeutic proteins

  • Ingested materials

*food, orally administered drugs

  • Contacted materials

*leaves, industrial products made from plants, synthetic chemicals, metals

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5
Q

Common properties of allergens

A
  • Relatively small
  • Highly soluble
  • Often carried on dessicated particles
  • Often proteases
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6
Q

When activated, Th2 cells secrete

A
  • IL-4; favor Ig class switching to IgE, stimulates Th2 differentiation
  • IL-5; activates eosinophils
  • IL-6
  • IL-10
  • IL-13; promotes IgE production and mucus secretion
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7
Q

IgE binds to

A
  • FcRepsilon on mast cell and basophils; sensitizes the individual
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8
Q

First wave of meadiators (pre-formed) in allergic reaction

A
  • Histamine

*acts on receptors (H1, H2, H3); H1 probably most important in allergic responses

*acts on: smooth muscle: contraction, blood vessel endothelium: causing increased vascular permeability and inflammation, epithelium of mucosa: mucus production

  • Heparin: anti-coagulant
  • Chondroitin sulfate
  • Enzymes: neutral proteases and acid hydrolases, cause tissue damage; lead to the production of kinins and activated complement components (such as C3a)
  • TNF-a: mast cells are only cells that can store, acts in concert w/histamine; activated endothelial cells, increases expression of adhesion molecules
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9
Q

Second wave of mediator (synthesized de novo) in allergic reaction

A
  • Chemokines
  • Cytokines: IL-4, TNF-a
  • Prostaglandin D2:

*most abundant mediator produced in mast cells by the cyclooxygenase pathway

*promotes dilation and increased vascular permeability: mucus secretion

*intense bronchospasm

*chemoattractant for neutrophils

  • Leukotrienes C4 and D4 are the most potent and spasmogenic agents known

*activities similar to histamine, only about 100-1000x more potent

*inflammation

*smooth muscle contraction

*airway constriction (smooth muscle contraction)

*mucus secretion

  • Leukotriene B4: highly chemotactic for neutrophils, eosinophils and monocytes
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10
Q

Type II hypersensitivity disorders are mediated by

A
  • Antibodies directed against antigens present in:

*cell surfaces

*ECM

*may be intrinsic to the cell membrane or matrix

*may be an exogenous antigen (such as a drug metabolite) that is absorbed onto the cell or matrix

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11
Q

3 Different mechanisms for Type II Hypersensitivity

A
  1. Phagocytosis mediated by opsonization (via complement or antibody)
  2. Complement and Fc-receptor mediated inflammation
  3. Antibody mediated cellular disfunction
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12
Q

Antibody-dependent cellular cytotoxicity

A
  • Plays a role in Type II hypersensitivity
  • Cells coated w/low level of IgG can be killed by a variety of effector cells. Effector cells bind to the antibody-coated target cell via FcgammaR. These effector cells include:

*monocytes

*neutrophils

*eosinophils

*NK cells

  • In ADCC, cell lysis proceeds w/o phagocytosis
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13
Q

Diseases in which Type II hypersensitivity plays a prominent role include

A
  • Transfusion reactions
  • Hemolytic disease of the newborn
  • Autoimmune hemolytic anemia, agranulocytosis and thrombocytopenia (individuals make autoimmune antibodies directed against their own blood cells)
  • Certain drug reaction in which the drug binds to the surface of a cell, usually by complexing to some host cell protein, and creates a foreign epitope to which antibodies can be generated
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14
Q

Rhogam

A
  • Sterile preparation of IgG specific for the RhD antigen
  • Given to all Rh- mother at 28 weeks gestation and again within 72hrs of delivery
  • The IgG will bind to any fetal RBC that have entered the maternal circulation and opsonizes them for clearance before the mother can mount her own immune response

*while IgG can cross the placent, it is though that, despite this fact the amount of immunoglobin that is given therapeutically is insufficient to cause destruction of fetal erythrocytes but is sufficent to clear any fetal RBC in the maternal circulation

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15
Q

Type II hypersensitivity disease chart

A
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16
Q

Type III hypersensitivity

A
  • Antigen-antibody complexes produce tissue damage mainly by eliciting inflammation at the sites of deposition. Typically, Type III hypersensitivites when antigen combines w/antibody within the circulation as circulating immune complexes, which then often deposit into vessel walls
  • Some the immune complexes are formed within tissue
  • The antigens that elicit Type III reactions can be exogenous protein or endogenous protein, in which case the reaction is autoimmune
17
Q

Immune complexes bind to inflammatory cells through

A
  • FcR on C3bR
18
Q

Clinical signs assoc. w/ deoposition of immune complexes in the tissue and induction of an inflammatory reaction

A
  • Fever
  • Urticaria
  • Arthralgias
  • Proteinuria
  • Lymphadenopathy
19
Q

Type III hypersensitivity disease chart

A

CMBM Exam 4 (14 decks)

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