Rituximab targets CD20 on B-lymphocytes. CD20 is absent on plasma cells; this explains why rituximab:
- A Causes permanent humoral immunodeficiency because it eliminates all B-cell precursors and memory cells
- B Requires a loading dose because plasma cells rapidly regenerate CD20-positive B-cells
- C Is combined with daratumumab (anti-CD38) in CLL to cover the CD20-negative plasma cell population
- D Is ineffective in multiple myeloma, which is a plasma cell neoplasm, but effective in follicular lymphoma and CLL ✓
Explanation
CD20 is expressed on pre-B-cells and mature B-lymphocytes but is absent on pro-B-cells and fully differentiated plasma cells. Rituximab depletes the CD20-positive B-cell lineage (useful in follicular lymphoma, DLBCL, CLL, and autoimmune diseases) but cannot target plasma cells, which is why it has no role in multiple myeloma (daratumumab targets CD38 on plasma cells). B-cell reconstitution occurs from CD20-negative precursors, so immunodeficiency is not permanent.
Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.
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Written and medically reviewed by the StethoPrep medical team.