The mechanism by which a Type III hypersensitivity reaction causes glomerulonephritis in post-streptococcal disease involves:
- A Deposition of circulating immune complexes (antigen-antibody) in glomeruli, activating classical complement pathway and recruiting neutrophils via C5a ✓
- B Direct deposition of streptococcal M-protein in glomerular basement membrane activating complement via alternative pathway
- C Molecular mimicry between streptolysin O and glomerular antigens stimulating autoreactive T-cells
- D IgE-mediated mast cell degranulation in glomerular capillaries releasing histamine
Explanation
Post-streptococcal glomerulonephritis is the classic Type III (immune complex-mediated) hypersensitivity. Circulating immune complexes of streptococcal antigens (e.g., endostreptosin, streptokinase) with IgG antibodies deposit in glomerular subepithelial or mesangial locations. Classical complement activation generates C3a and C5a; C5a is a potent neutrophil chemoattractant. Neutrophil-released proteases and reactive oxygen species damage the glomerular basement membrane. Immunofluorescence shows granular ('lumpy-bumpy') C3 and IgG deposits.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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