Rituximab depletes CD20-positive B cells by multiple mechanisms. Which effector mechanism accounts for most of its clinical activity and depends on the Fc portion engaging NK cells bearing CD16?

• A Complement-dependent cytotoxicity
• B Induction of apoptosis by cross-linking surface CD20
• C Antibody-dependent cellular cytotoxicity ✓
• D Inhibition of B cell receptor signalling

Explanation

ADCC occurs when rituximab Fc binds Fc-gamma receptor III (CD16) on NK cells, triggering perforin-granzyme killing of the opsonised lymphoma cell. Complement lysis contributes, especially to early infusion reactions, and direct apoptosis and calcium flux occur in vitro, but ADCC is considered the dominant in-vivo mechanism. Obinutuzumab was glycoengineered specifically to enhance Fc-gamma receptor binding and strengthen ADCC over rituximab.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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