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Pharmacology · Chemotherapy: abatacept mechanism
Sample itemA patient with rheumatoid arthritis not controlled by methotrexate is started on abatacept, a fusion protein of CTLA-4 and the Fc portion of IgG1. How does it work?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
C. Binding CD80 and CD86, blocking T-cell co-stimulation
Abatacept binds CD80 and CD86 on antigen-presenting cells, so they cannot engage CD28 on T cells and the co-stimulatory signal for T-cell activation is lost. Rituximab depletes CD20-positive B cells, tocilizumab blocks the IL-6 receptor, and tofacitinib inhibits JAK enzymes.
Option by option
A. Inhibition of Janus kinases in lymphocytes
JAK inhibition is the action of tofacitinib.
B. Depletion of B cells by binding CD20
B-cell depletion through CD20 is the action of rituximab.
C. Binding CD80 and CD86, blocking T-cell co-stimulation (correct)
Correct. Abatacept blocks CD28 co-stimulation by binding CD80 and CD86.
D. Blockade of the interleukin-6 receptor
IL-6 receptor blockade is the action of tocilizumab.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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