In Type II hypersensitivity reactions, tissue injury can occur by which three mechanisms?
- A IgE-mediated mast cell degranulation, T-cell cytotoxicity, and immune complex deposition
- B Complement activation, ADCC, and receptor blockade/dysfunction by antibodies ✓
- C Immune complex deposition, neutrophil recruitment, and complement activation only
- D CD8+ T-cell cytotoxicity, NK cell killing, and delayed-type hypersensitivity
Explanation
Type II hypersensitivity is antibody-mediated (IgG or IgM against cell surface or matrix antigens) and causes injury via: (1) complement activation leading to lysis or opsonization, (2) antibody-dependent cellular cytotoxicity (ADCC) by NK cells, and (3) non-cytolytic antibody binding to receptors causing dysfunction (e.g., TSH receptor stimulation in Graves' disease or nicotinic receptor blockade in myasthenia gravis). IgE and mast cells are Type I; immune complexes characterize Type III.
Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.
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