Rituximab is a chimeric anti-CD20 monoclonal antibody. The predominant mechanism by which rituximab kills B cells in lymphoma is:

• A Complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC) ✓
• B Direct apoptosis induction via intracellular signaling through CD20
• C Blockade of B cell receptor (BCR) signaling via CD20-mediated receptor internalization
• D Recruitment of CD8+ T cells to lyse CD20-expressing cells via ADCP only

Explanation

Rituximab kills CD20-positive B cells through two main effector mechanisms. First, the Fc region of bound rituximab activates complement (C1q binding), leading to membrane attack complex (MAC) formation and complement-dependent cytotoxicity (CDC). Second, NK cells, macrophages, and neutrophils bind the Fc region via FcgammaRIII, killing opsonized B cells by antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP). CD20 itself does not transduce intracellular signals and is not internalized upon antibody binding, distinguishing it from receptor-targeting antibodies.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.