Pathology · Immunopathology (Hypersensitivity, Autoimmunity, Immunodeficiency, Amyloidosis)

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
Correct answer: B. Complement activation, ADCC, and receptor blockade/dysfunction by antibodies

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.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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