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Abstract：
With the inception of the Edmonton Protocol, intraportal islet transplantation (IPIT) has re-emerged as a promising cell-based therapy for type 1 diabetes. However, current clinical islet transplantation remains limited, in part, by the need to transplant islets from 2-4 donor organs, often through several separate infusions, to reverse diabetes in a single patient. Results from clinical islet transplantation and experimental animal models now indicate that the majority of transplanted islets are destroyed in the immediate post-transplant period, a process largely facilitated by deleterious inflammatory responses triggered by islet-derived procoagulant and proinflammatory mediators. Herein, mechanisms that underlie the pathophysiology of thrombosis and inflammation in IPIT are reviewed, and emerging approaches to improve islet engraftment through attenuation of inflammatory responses are discussed.
摘要：
随着《埃德蒙顿议定书》的出台,视网膜内胰岛移植(IPIT)已重新成为治疗1型糖尿病的一种有前景的基于细胞的疗法.然而,目前临床胰岛移植仍然有限，在某种程度上,需要移植2-4个供体器官的胰岛，通常通过几次单独的输液，在单个患者中逆转糖尿病。目前，临床胰岛移植和实验动物模型的结果表明，大多数移植的胰岛在移植后立即被破坏，该过程主要由胰岛来源的促凝血和促炎介质触发的有害炎症反应促进。在这里，综述了IPIT中血栓形成和炎症病理生理学的基础机制，讨论了通过减轻炎症反应来改善胰岛植入的新兴方法。
