A 28-year-old woman with systemic lupus erythematosus has elevated anti-dsDNA antibody titres and low complement levels. Kidney biopsy shows subendothelial immune deposits and wire-loop lesions. Which complement pathway is PRIMARILY activated by immune complexes deposited in glomeruli?
- A Classical pathway via C1q binding to Fc regions ✓
- B Lectin pathway via MASP-2
- C Alternative pathway via spontaneous C3 hydrolysis
- D Terminal pathway bypassing C3 cleavage
Explanation
Immune complex–mediated glomerulonephritis (WHO Class III/IV lupus nephritis) is a classic Type III hypersensitivity reaction in which IgG-containing immune complexes activate the classical complement pathway by binding C1q through Fc regions of IgG, generating C3a and C5a. C3a and C5a are anaphylatoxins and chemotaxins that attract neutrophils, causing tissue damage. The lectin pathway is activated by mannose residues, and the alternative pathway is triggered by certain microbial surfaces, neither of which is primary here. Low C3/C4 reflect classical-pathway consumption.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.