## Distinguishing Type II from Type III Hypersensitivity ### Core Mechanism Difference **Key Point:** Type II hypersensitivity is characterized by **direct antibody binding to cell surface antigens**, whereas Type III involves **soluble antigen-antibody complexes** deposited in tissues. ### Comparison Table | Feature | Type II (Cytotoxic) | Type III (Immune Complex) | | --- | --- | --- | | **Target** | Cell surface antigens | Soluble circulating antigens | | **Antibody binding** | Direct to cell membrane | Indirect via immune complexes | | **Primary mechanism** | Antibody-dependent cellular cytotoxicity (ADCC), complement activation on cell surface | Immune complex deposition in vessel walls, joints, kidneys | | **Circulating immune complexes** | Absent or minimal | Present and elevated | | **Cell damage** | Extracellular lysis of target cells | Tissue inflammation at deposition sites | | **Examples** | Graves' disease, Goodpasture syndrome, pemphigus vulgaris | Serum sickness, SLE, post-streptococcal GN | ### Why Option 1 Is Correct **High-Yield:** Direct IgG binding to cell surface antigens is the **hallmark of Type II hypersensitivity**. This antibody-antigen interaction on the cell membrane triggers: - Complement activation (C1q binding) - ADCC via Fc receptors on NK cells and macrophages - Opsonization and phagocytosis This distinguishes it fundamentally from Type III, where antibodies bind to **soluble antigens in circulation** before complex deposition. ### Clinical Pearl In **Graves' disease** (Type II), anti-TSH receptor IgG directly binds thyroid cell surface receptors → thyroid stimulation. In **serum sickness** (Type III), antigen-antibody complexes circulate → deposit in skin, joints, kidneys → inflammation. [cite:Robbins 10e Ch 6]
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