An exaggerated or inappropriate immune response that causes tissue damage.
Type 1 (IgE crosslinking on mast cells)
- Plasma cells stimulated by antigen \(\to\) produce IgE
- IgE coats mast cells
- Re-exposure to antigen \(\to\) crosslinks IgE \(\to\) mast cell degranulation \(\to\) histamine, bradykinin, mast cell trypase release
- These products directly cause vasodilation, increased permiability (\(\therefore\)angioedema) and bronchoconstriction \(\to\) early phase response at ~5 minutes
- Cause chemotaxis of eosinophils, neutrophils, lymphocytes \(\to\) inflammation \(\to\) late phase response at ~4 hours
- E.g. asthma, anapylaxis
Type 2 (Ig-cell surface interaction)
- Antibody produced against self-antigen on a cell surface
- Antibody binds to cell
- Cell destroyed by compliment, or by antibody-dependant immune cell activity (e.g. neutrophil degranulation)
- e.g. ABO incompatibility
Type 3 (Immune complex formation)
- Antigen excess \(\to\) excessive antigen-antibody complexes \(\to\) chemotaxis, local inflammation
- e.g. SLE
Type 4 (Delayed, cell-mediated immunity)
- Antigens presented to Th1 cells \(\to\) clonal profileration \(\to\) cytokines \(\to\) macrophage overactivity \(\to\) tissue damage
- E.g contact dermatitis