Graft rejection prevention

Graft rejection prevention refers to the clinical use of immunosuppressive drugs and biologic agents to stop the immune system from attacking transplanted organs or stem cells. The underlying biology involves blocking T cell–mediated recognition, activation, and destruction of the transplanted tissue, as well as suppression of humoral responses such as antibody formation[1][2][4][5][6]. Common immunosuppressant drug classes include calcineurin inhibitors (tacrolimus, cyclosporine), corticosteroids (prednisone), nucleotide synthesis inhibitors (mycophenolate mofetil, azathioprine), mTOR inhibitors (sirolimus, everolimus), and monoclonal antibodies (basiliximab, anti-thymocyte globulin)[1][5][7][3][4]. Each drug targets specific molecules or pathways involved in immune activation such as interleukin-2 (IL-2) signaling, T cell receptor complexes, or B cell activation[1][3][4][5][7]. Patients requiring graft rejection prevention are typically monitored for immune cell activity and graft function; tissue biopsies, circulating biomarkers (such as donor-specific antibodies), and drug levels help assess efficacy and safety, but these measurements do not indicate a single druggable molecular target[5][6]. Key context: The term "graft rejection prevention" should not be used as a drug target; rather, specific molecular targets (such as "Interleukin-2 receptor alpha" or "Calcineurin") should be referenced in therapeutic contexts. Drugs are designed to prevent rejection by inhibiting these real molecular targets.

Other names

Graft rejectionAllograft rejectionTransplant rejection preventionAntirejection