Final answer:
Mycophenolate mofetil prevents organ rejection by inhibiting the proliferation of T cells through reversible inhibition of the enzyme IMPDH, essential for synthesizing guanosine nucleotides in lymphocytes. This differs from cyclosporine, which inhibits cytokine production to suppress T cell activation.
Step-by-step explanation:
Mycophenolate mofetil is a medication used to prevent rejection of transplanted organs, similar to the drug cyclosporine. It functions by inhibiting a crucial pathway necessary for the proliferation of T cells, which are a type of white blood cell involved in the immune response. The specific action of mycophenolate mofetil is the reversible inhibition of inosine monophosphate dehydrogenase (IMPDH), an enzyme that is important for the synthesis of guanosine nucleotides in lymphocytes.
Without these nucleotides, the T cells cannot proliferate and therefore cannot attack the transplanted organ. Mycophenolate mofetil acts selectively on lymphocytes because they rely heavily on the de novo synthesis pathway, in which IMPDH plays a key role, for their proliferation. Unlike other cell types, lymphocytes lack a salvage pathway that could bypass this blockade. The result is a reduced immune response and a lower risk of organ rejection.
As a comparison, cyclosporine suppresses the immune system through a different mechanism. It inhibits the production of interleukin-2 and other cytokines, which are essential for the activation and growth of T cells. Both medications, however, are used to achieve a similar goal: reducing the likelihood of transplant rejection.