ciclosporin's main effect is to lower the activity of t-cells; it does so by inhibiting calcineurin in the calcineurin–phosphatase pathway and preventing the mitochondrial permeability transition pore from opening. ciclosporin binds to the cytosolic protein cyclophilin (immunophilin) of lymphocytes, especially of t cells. this cyclosporin—cyclophilin complex inhibits calcineurin, which is normally responsible for activating the transcription of interleukin 2. in t-cells, activation of the t-cell receptor normally increases intracellular calcium, which acts via calmodulin to activate calcineurin. calcineurin then dephosphorylates the transcription factor nf-at (nuclear factor of activated t-cells), which moves to the t-cell nucleus and increases the transcription of genes for il-2 and related cytokines. ciclosporin, by preventing the dephosphorylation of nf-at, leads to reduced effector t-cell function; it does not affect cytostatic activity.