A 28-year-old woman with SLE has persistent low C3 and C4 levels with recurrent infections by encapsulated bacteria. Which complement pathway deficiency best explains this combined clinical and serological pattern?

• A Terminal complement (C5–C9) deficiency
• B Mannose-binding lectin (MBL) deficiency
• C Properdin deficiency
• D Classical pathway component C2 deficiency ✓

Explanation

C2 deficiency is the most common complement deficiency and strongly associates with SLE due to impaired immune complex clearance via the classical pathway, which also consumes C3 and C4. Terminal complement deficiency (C5–C9) predisposes to Neisseria infections, not SLE. MBL deficiency causes recurrent childhood infections but is not linked to SLE. Properdin deficiency impairs the alternative pathway and predisposes specifically to meningococcal disease.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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