Final answer:
Cyclosporin A inhibits interleukin-2 synthesis, primarily affecting T-helper cells and cytotoxic T lymphocytes (CTLs), which play key roles in immune responses, including organ transplant rejection.
Step-by-step explanation:
The drug cyclosporin A is utilized in organ transplantation to prevent rejection by specifically inhibiting the synthesis of interleukin-2 (IL-2), a critical cytokine in the immune response. IL-2 predominantly acts on T cells, particularly contributing to the proliferation and activation of various T cell subsets, including T-helper (Th) cells and cytotoxic T lymphocytes (CTLs). By inhibiting IL-2, cyclosporin A hinders the activity of these T cells, effectively reducing immune responses against the transplanted organ.
Among the T cells affected, CTLs are specifically integral in transplant rejection because they can directly target and kill cells that are perceived as foreign, such as those in a transplanted organ. Similarly, Th cells provide crucial support to other immune cells, and their suppression also plays a role in reducing organ rejection. Therefore, the gross effect of IL-2 inhibition is a dampening of the body’s immune response that could otherwise lead to the destruction of the transplanted tissue.