## Distinguishing Type II from Type III Hypersensitivity ### Core Mechanism Difference **Key Point:** Type II hypersensitivity involves **direct antibody binding to cell surface antigens**, whereas Type III involves **circulating immune complex deposition** in tissues. ### Comparative Table | Feature | Type II (Cytotoxic) | Type III (Immune Complex) | | --- | --- | --- | | **Antibody target** | Cell surface antigens | Soluble antigens (circulating) | | **Mechanism** | Direct IgG/IgM binding → complement activation → cell lysis | Immune complex formation → deposition in vessels/tissues → inflammation | | **Site of injury** | Cell membrane (target cell) | Vessel walls, joints, glomeruli, skin | | **Pathology** | Cytolysis, cell destruction | Vasculitis, arthritis, glomerulonephritis | | **Examples** | Graves' disease, autoimmune hemolytic anemia, Goodpasture syndrome | Serum sickness, SLE, post-streptococcal GN | ### Why This Feature Discriminates **High-Yield:** In Type II, antibodies **directly recognize and bind to cell surface epitopes** (e.g., thyroid peroxidase in Graves', RBC membrane in AIHA). This direct cell-surface binding is the pathognomonic feature and distinguishes it from Type III, where antibodies bind to soluble antigens in circulation, forming complexes that subsequently deposit in tissues. ### Clinical Pearl **Clinical Pearl:** Type II reactions are **cell-targeted** (the cell itself is the enemy); Type III reactions are **tissue-targeted** (immune complexes rain down on innocent bystander tissues). ### Mnemonic **Mnemonic:** **DIRECT vs. DEPOSIT** — Type II = DIREct cell binding; Type III = DEPOSITion in tissues. [cite:Robbins 10e Ch 6]
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