HYPERSENSITIVITY-Summary

Immediate Hypersensitivity: Mediated by IgE antibodies, mast cells, and eosinophils (type I)
Cytotoxic Hypersensitivity: Mediated by IgM or IgG antibodies (type II)
Immune-Complex Hypersensitivity: Mediated by antigen-antibody complexes deposited in tissue. (type III)
Delayed Hypersensitivity: Mediated by helper T cells and macrophages. Independent of antibodies. (type IV)

MECHANISMS

****Immediate Hypersensitivity (TYPE I) : Initial exposure leads to antibody synthesis and memory B-Cell production

Re-exposure: Antigen causes production of IgE antibodies.
HOW?? Allergens presented by B cells activate Helper T-cells. Helper T-cells
Release cytokines that cause B cells to turn into IgE-producing plasma cells.
⇒ IgE antibodies become attached to mast cells via binding sites on their Fc portions (cross over is important) -> Same antigen binds to IgE bound to mast cell and inflammatory mediators are activated (histamines, eicosanoids, chemokines) SEE DIAGRAM












Cytotoxic Hypersensitivity:















Immune-Complex Hypersensitivity:
-Many antibodies (IgG or IgM) combine with free antigens
-> antigen-antibody complexes precipitate out on the surface of endothelial cells or become trapped in capillary walls
-> complexes activate complement system (several proteins work together to kill target cells) and inflammatory response occurs

Delayed Hypersensitivity:
-Antigens in the area activate cytokines via helper T cells
-> cytokines act as inflammatory mediators and activate macrophages to secrete their potent mediators.
-> allergy develops in several days