TGF-BETA IN RENAL-ALLOGRAFT REJECTION

The role of TGF-beta in pathological processes in the transplanted kid ney is beginning to be investigated both in animal models and in human s. In both settings in acute cell-mediated rejection, TGF-beta, recept or, and message have all been documented to be elevated in the tubuloi nterstitium, likely a reflection of TGF-beta's role in recruiting leuk ocytes to areas of injury and downregulation of the inflammatory respo nse. In chronic rejection, expression of TGF beta, message, and induce d proteins is elevated, especially in cortex. TGF-beta mRNA, unlike ot her inflammatory cytokine mRNAs, correlated very well with interstitia l fibrosis, a hallmark of chronic rejection. Thus, a relationship betw een renal scarring and TGF-beta has been documented by most studies of transplant kidneys. Additionally, this growth factor also appears to have a role in the renal fibrosis associated with cyclosporine adminis tration and perhaps in augmenting this drug's immunosuppressive effect s.