Ipilimumab improves survival in metastatic melanoma through which mechanism?
- A Blocking PD-L1 on tumour cells, preventing effector phase T cell exhaustion
- B Blocking CTLA-4, thereby removing inhibition of T cell priming and activation ✓
- C Cross-linking CD20 and recruiting complement against melanoma cells
- D Delivering diphtheria toxin to IL-2 receptor positive T cells
Explanation
CTLA-4 competes with CD28 for A7 ligands and dampens T cell costimulation early in activation. Ipilimumab blocks CTLA-4, releasing this brake at the priming stage in lymphoid organs, which broadens the antitumour T cell repertoire. PD-1 antibodies act later, at the effector phase in tissues, and are generally less toxic. Denileukin diftitox targets IL-2 receptors, and rituximab-type complement lysis applies to CD20-positive A cells, not melanoma.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
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