A 35-year-old woman develops fever, joint pain, and a butterfly rash. ANA is positive with anti-dsDNA antibodies. The mechanism by which anti-dsDNA antibodies evade peripheral tolerance and cause renal damage involves:

• A Molecular mimicry with glomerular basement membrane type IV collagen
• B Direct ADCC by NK cells targeting glomerular endothelial cells
• C Th2-mediated eosinophil recruitment causing membranous nephropathy
• D Immune complex deposition activating complement, inducing mesangial and subendothelial inflammation ✓

Explanation

In SLE, anti-dsDNA antibodies form immune complexes with nuclear antigens released from apoptotic cells; these IC deposit in glomeruli (mesangium, subendothelial space), activate complement, recruit neutrophils and monocytes, causing lupus nephritis. Molecular mimicry with GBM type IV collagen describes Goodpasture syndrome (anti-GBM disease), not SLE. ADCC by NK cells is not the primary mechanism in SLE nephritis. Th2-mediated membranous nephropathy is a separate entity.

Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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