作者: Faouzi Braza , Sophie Brouard , Steve Chadban , Daniel R. Goldstein
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摘要: Graft inflammation impairs the induction of solid organ transplant tolerance and enhances acute chronic rejection. Elucidating mechanisms by which is induced after transplantation could lead to novel therapeutics improve outcomes. In this Review we describe endogenous substances--damage-associated molecular patterns (DAMPs)--that are released allograft reperfusion induce inflammation. We also innate immune signalling pathways that activated transplantation, with a focus on Toll-like receptors (TLRs) their signal adaptor, MYD88. Experimental clinical studies have yielded large body evidence TLRs MYD88 instrumental in initiating promoting development Ongoing testing TLR inhibition strategies although avoiding compromising host defence pathogens key challenge. Further elucidation sterile induced, maintained amplified within has potential anti-inflammatory treatments outcomes for recipients.