Calcineurin inhibitors primarily prevent activation of which immune cells involved in graft rejection?

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Multiple Choice

Calcineurin inhibitors primarily prevent activation of which immune cells involved in graft rejection?

Explanation:
Calcineurin inhibitors block a crucial step in T cell activation. When a T cell recognizes donor antigens, calcineurin activates and dephosphorylates NFAT, allowing NFAT to enter the nucleus and drive transcription of interleukin-2. IL-2 is the key growth signal that promotes T cell clonal expansion. By inhibiting calcineurin, these drugs prevent IL-2 production, so T cells don’t proliferate and the cell-mediated response driving graft rejection is reduced. The primary effect is on T lymphocytes; neutrophils and eosinophils aren’t the main targets, and while B cells can be affected indirectly via diminished T helper support, the standout action is on T cells.

Calcineurin inhibitors block a crucial step in T cell activation. When a T cell recognizes donor antigens, calcineurin activates and dephosphorylates NFAT, allowing NFAT to enter the nucleus and drive transcription of interleukin-2. IL-2 is the key growth signal that promotes T cell clonal expansion. By inhibiting calcineurin, these drugs prevent IL-2 production, so T cells don’t proliferate and the cell-mediated response driving graft rejection is reduced. The primary effect is on T lymphocytes; neutrophils and eosinophils aren’t the main targets, and while B cells can be affected indirectly via diminished T helper support, the standout action is on T cells.

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