Recallab › Question bank › Pathology › Immunity › #50122
Basiliximab
A patient receiving a renal transplant is given basiliximab as induction therapy. What is its mechanism of action?
- A. It binds CD3 on all T cells and causes their depletion
- B. It inhibits mTOR and blocks the response to interleukin-2
- C. It inhibits calcineurin and blocks interleukin-2 transcription
- correctD. It binds CD25, the alpha chain of the interleukin-2 receptor on activated T cells
Explanation
Key fact
Basiliximab blocks the IL-2 receptor (CD25) on activated T cells - it stops the cells that are already responding to the graft, and leaves the rest alone.
It binds CD25, the alpha chain of the interleukin-2 receptor. Only activated T cells express it, so the drug is unusually selective.
Why
A T cell recognising the graft makes interleukin-2 and upregulates its receptor.
The high-affinity receptor needs the alpha chain, CD25.
Basiliximab is a chimeric monoclonal antibody against CD25.
Occupying it stops the autocrine loop that drives clonal expansion.
Resting T cells barely express CD25, so they are untouched - hence few side effects.
Where the transplant drugs act
| Drug | Target |
|---|---|
| Basiliximab | CD25, the IL-2 receptor alpha chain |
| Muromonab (anti-CD3) | CD3 on all T cells |
| Ciclosporin, tacrolimus | Calcineurin, blocking IL-2 transcription |
| Sirolimus | mTOR, blocking the response to IL-2 |
| Mycophenolate | Inosine monophosphate dehydrogenase |
Three drugs, one pathway, three different places to stop it
Why not the others
- A. It binds CD3 on all T cells and causes their depletion — is muromonab. This is the answer one circulating recall gives for basiliximab, and it is wrong.
- B. It inhibits mTOR and blocks the response to interleukin-2 — is sirolimus, which acts downstream of the receptor.
- C. It inhibits calcineurin and blocks interleukin-2 transcription — is ciclosporin and tacrolimus - they stop IL-2 being made, upstream of the receptor.
Remember
Three drugs, three points on one pathway. Tacrolimus stops the signal being made, basiliximab stops it being received, sirolimus stops it being obeyed.
Go deeper
Induction agents are given at the time of transplant to cover the period of highest rejection risk, then stopped; maintenance immunosuppression continues indefinitely.
Because it spares resting lymphocytes, basiliximab does not cause the cytokine release syndrome that made anti-CD3 antibodies difficult to use.
Robbins, Cotran & Kumar Pathologic Basis of Disease, 11th ed. (Elsevier, 2025); Katzung's Basic & Clinical Pharmacology, 16th ed. (McGraw Hill, 2024).