hypersensitivity Flashcards
triggers of hypersensitivity
- SELF ANTIGENS- autoimmunity 2. MICROBIAL ANTIGENS- excessive inflammation 3. ENVIRONMENTAL- allergy
persistent triggers of hypersensitivity can lead to
chronic disease
hypersensitivity
defect in regulation or targeting of the usually beneficial immune response
type I hypersensitivity
- immediate, IgE-mediated, allergy - within minutes - involve antigen specific IgE on effector cells - vasoactive mediators, lipid mediators, cytokine - HISTAMINE
examples of type I hypersensitivity
- allergic rhinitis (hay fever) - atopic asthma - anaphylaxis (food allergy, stinging insect allergy, drug allergy)
type I, II, and III hypersensitivity similarities
mediated by antibodies
type II and III hypersensitivity involve which antibodies
IgG and IgM
Type II hypersensitivity
- injury related to antibody directly bing to target - minutes to hours - antigens are specific cells are extracellular matrix - local tissue/cell specific
Type III hypersensitivity
- injury related to immune complex deposition - antigens are present in circulation - systemic
which class of immunoglobulin is most abundant in the bloodstream?
IgG
IgG
- neutralization of microbes and toxins - most abundant in the bloodstream - opsonization of antigens for phagocytosis by macrophages and neutrophils - activation of the classical pathway of complement - neonatal immunity - activates NK cells
IgM
activation of the classical pathway of complement
IgA
- mucosal immunity - neutralizations of toxins
IgE
eosinophils and mast cell mediated defense against helminths
type II hypersensitivity mechanism
antibodies causing 1. opsonization/phagocytosis 2. complement/Fc receptor inflammation 3. receptor activation
goodpasture syndrome
- anti-glomelular basement membrane disease
- antibodies against basement membrane in kidney and lung
- fatigue, blood in the ling, bloody urine, kidney failure

idiopathic thrombocytopenic purpure (ITP)
- autoantibodies against platelets –> opsonization in the slpeen

normal

autoimmune hemolytic anemia
- autoantibodies against RBC membrane proteins
type II hypersensitivity
- antibody stimulates the receptor without hormone
- antibody inhibits binding of neurotransmitter to receptor
- antibody binds antigen and attracts neutrophils and or complement which leads to inflammation
- antibody coats outside of cells and then phagocytes come and eat them
acute rheumatic fever, pemphigus vulgaris, pernicious anemia are clinical examples of type I or type II hypersensitivities
II
timing of type III hypersensitivtiy
3-10 hours
immune complex mediated hypersensitivity
Type III
mechanism of Type III hypersensitivity
antibodies bind appropriate sized antigens and deposit in vessels or tissue cause complement/Fc receptor inflammation
- causes vaculitis