TGF-beta in renal allograft rejection.
The role of TGF-beta in pathological processes in the transplanted kidney is beginning to be investigated both in animal models and in humans. In both settings in acute cell-mediated rejection, TGF-beta, receptor, and message have all been documented to be elevated in the tubulointerstitium, likely a reflection of TGF-beta's role in recruiting leukocytes to areas of injury and downregulation of the inflammatory response. In chronic rejection, expression of TGF-beta, message, and induced proteins is elevated, especially in cortex. TGF-beta mRNA, unlike other inflammatory cytokine mRNAs, correlated very well with interstitial fibrosis, a hallmark of chronic rejection. Thus, a relationship between 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 administration and perhaps in augmenting this drug's immunosuppressive effects.
Cohen
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Department of Pathology, Cedars-Sinai Medical Center, UCLA School of Medicine, Los Angeles, Calif 90048, USA. cohena@CSMC.EDU
Nast
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D000818:Animals; D016572:Cyclosporine / Q000633:toxicity; D006084:Graft Rejection; D006801:Humans; D007166:Immunosuppressive Agents; D016030:Kidney Transplantation; D012333:RNA, Messenger / Q000378:metabolism; D018125:Receptors, Transforming Growth Factor beta / Q000502:physiology; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000502:physiology*
D007166:Immunosuppressive Agents; D012333:RNA, Messenger; D018125:Receptors, Transforming Growth Factor beta; D016212:Transforming Growth Factor beta; D016572:Cyclosporine