In systemic lupus erythematosus (SLE), anti-dsDNA antibodies contribute to glomerulonephritis primarily by:

• A Direct binding to GBM structural proteins causing complement-independent lysis
• B Activating autoreactive T cells that directly attack mesangial cells
• C Cross-reacting with podocyte surface antigens, causing foot process effacement
• D Forming circulating immune complexes with dsDNA that deposit in glomeruli, activate complement, and recruit inflammatory cells ✓

Explanation

In lupus nephritis, DNA released from apoptotic cells binds anti-dsDNA IgG to form immune complexes in the circulation; these deposit in the mesangium and subendothelial/subepithelial spaces, activate complement via the classical pathway (generating C3a, C5a), recruit neutrophils and monocytes, and cause glomerular injury. The pattern on IF is 'full-house' (IgG, IgM, IgA, C3, C1q).

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.