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  • Title: Roles of toll-like receptors signaling in organ transplantation.
    Author: Li T, Chen G, Zhang Z.
    Journal: Zhong Nan Da Xue Xue Bao Yi Xue Ban; 2011 Dec; 36(12):1125-33. PubMed ID: 22246357.
    Abstract:
    Organ transplantation is the gold standard of treatment for patients with end-stage organ failure. However, transplant recipients must take immunosuppressive drugs lifelong to fight against rejection, which is inevitably caused by the recipient's immune system in response to transplanted foreign tissues. Despite advances in the prevention of acute rejection, it is still a significant and potentially devastating complication of solid organ transplantation. Moreover, chronic allograft dysfunction as a result of acute and chronic alloimmune-mediated injury still develops in a majority of transplant recipients regardless of continuous immunosuppression. While host adaptive immune responses elicited by T lymphocytes are primarily responsible for allotransplant rejection, emerging evidence supports an important role of the innate immune system in the development of organ rejection. Innate immune recognition is initiated by a set of diverse receptors that belong to different protein families including the family of toll-like receptors (TLRs). TLR signaling is a highly specialized system that can identify a variety of microbial and endogenous mediators, and activate the innate immune system in response to danger. The discovery of TLRs over the past 10 years has started a new era in understanding the molecular events that initiate and regulate the inflammatory response following organ transplantation. They influence the adaptive immune reactions and contribute to ischemic reperfusion injury, acute and chronic allograft rejection, and tolerance induction. Their role as potential targets for therapeutic intervention has just begun to be appreciated. In this article, we summarize the structural and functional characteristics of TLRs and their ligands. We focus on the studies to define the roles of TLRs in ischemic reperfusion injury, allotransplant rejection, and immune regulation in both animal models and clinical transplantation.
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