Hypersensitivity Flashcards
(41 cards)
triggered by environmental Ags, activates mast cells in an IgE-dependent manner
Type I Hypersensitivity
genetic tendency to develop allergic diseases
atopy
what are the five Type I mediators, and what are their functions?
- histamine: small vascular dilation, increase vascular permeability
- proteases: local tissue damage
- prostaglandins: vascular dilation
- leukotrienes: prolonged smooth muscle contraction
- cytokines: local inflammation (late-phase)
in Type I, what does primary exposure to the allergen result in?
activation of Th2 cells and production of IgE
in Type I, what does secondary exposure result in?
Ag-dependent cross-linking of membrane-bound IgE causing activation of mast cells –> release of inflammatory mediators
what are the characteristics of the immediate phase, which develops within minutes, in Type I?
vasodilation, congestion, edema
what are the characteristics of the late-phase reaction, which develops 2-24 hours later, in Type I?
inflammatory infiltrate, which is rich in eosinophils, neutrophils, and T cells
local reaction
asthma
inflammatory mediators from mast cells d/t allergen encounter; increase capillary permeability, spasmodic contraction of bronchs
non-immunologic stimuli includes cold and exercise
systemic reaction
anaphylaxis
d/t massive release of vasoactive amines and cytokines from mast cells – contraction of smooth m, vasodilation of capillary endothelium lowers BP and results in vascular shock while increasing difficulty of breathing
in Type II, which antibodies are responsible for activation of CP?
IgG, IgM
release of C3a and C5a during CP will result in inflammation via recruitment of leukocytes
in Type II, what inflammatory mediators are released from neutrophils and Mo in an Fc-dependent manner?
ROS, lysosomal enzymes
- will cause damage to adjacent tissues, inflammation
in Type II, Abs opsonize cells and lead to phagocytosis through which two receptors?
FcRy, CR1
drug-induced hemolytic anemias: drug binds directly to RBC surface, induces anti-drug Ab
Penicillin
drug-induced hemolytic anemias: auto-Ab form immune complexes w/ the drug
Quinidine
IC bind RBC via CR1
drug-induced hemolytic anemias: anti-drug Ab cross-reacts w/ Rh Ag
Methyldopa
manifestation of Type II: hemolysis, anemia
autoimmune hemolytic anemia
target Ag: RBC membrane pro
manifestation of Type II: bleeding
autoimmune (idiopathic) thrombocytopenia purpura
target Ag: platelet membrane pro
manifestation of Type II: nephritis, lung hemorrhage
Goodpasture’s syndrome
target Ag: non-collagenous pro in BM of kidney glomeruli and lung alveoli
manifestation of Type II: hyperthyroidism
Grave’s disease
target Ag: TSH receptor
manifestation of Type II: muscle weakness, paralysis
Myasthenia gravis
target Ag: ACH receptor
manifestation of Type II: skein vesicles (bull)
pemphigus vulgaris
target Ag: pro in IC jxns of epidermal cells
manifestation of Type II: abnormal erythropoiesis, anemia
pernicious anemia
target Ag: intrinsic factor of gastric parietal cells
manifestation of Type II: myocarditis, arthritis
Rheumatic fever
target Ag: step cell wall Ag; Ab cross-reacts w/ myocardial Ag
Ag-Ab IC formed in circulation and deposited in blood vessels and other tissues, including kidney and lungs
Type III Hypersensitivity
