Transplant Rejection
The immune system's attack on a transplanted organ or tissue, recognised as foreign. Preventing rejection requires lifelong immunosuppression. Cyclosporine revolutionised organ transplantation by enabling effective T cell suppression and remains a cornerstone of anti-rejection therapy.
Technical Context
Rejection types: hyperacute (minutes-hours — pre-formed antibodies against donor HLA antigens → complement activation → graft vessel thrombosis; prevented by crossmatch testing), acute cellular (days-months — T cell recognition of donor MHC → infiltration and destruction of graft tissue; treated with corticosteroids and T cell-directed immunosuppression), acute antibody-mediated (days-months — de novo anti-donor antibodies → complement activation → endothelial damage; treated with plasmapheresis, IVIG, rituximab), and chronic (months-years — progressive fibrosis and vasculopathy → gradual graft failure; poorly responsive to treatment). Cyclosporine revolutionised transplantation in the 1980s by providing effective T cell suppression — before cyclosporine, one-year kidney graft survival was approximately 50%; after its introduction, this rose to >80% and continues to improve with modern regimens. Current standard immunosuppression: calcineurin inhibitor (cyclosporine or tacrolimus) + antiproliferative (mycophenolate) + corticosteroid.