缺血再灌注肾损伤是导致移植排斥的重要原因，目前临床尚缺乏有效的治愈方法。免疫炎症是介导缺血再灌注肾损伤的主要因素。作为一种重要的促炎因子，我们前期结果发现：共刺激分子LIGHT及其受体HVEM和LTβR在小鼠缺血再灌注损伤肾组织中表达显著升高；反之，LIGHT基因缺陷缺血再灌注肾损伤则显著降低，提示：LIGHT通路可能在缺血再灌注肾损伤的病理发生中发挥关键作用。本研究拟在我们首次发现LIGHT缺陷可显著改善缺血再灌注肾损伤的基础上，通过体内外实验进一步探讨LIGHT通路介导缺血再灌注肾损伤的作用机制；评价阻断LIGHT通路在缺血再灌注肾损伤中的干预效果及其作用受体。预期结果不但有助于缺血再灌注肾损伤免疫病理机制的阐明，并可为缺血再灌注肾损伤临床治疗新策略的发展提供重要的理论依据。

Renal ischemia/reperfusion injury (IRI) is an unavoidable event during kidney transplantation，which is one of the critical causes that lead to graft rejection. There isn't an effective treatment strategy for patients with renal IRI. Numerous studies have revealed that inflammatory processes mediated by the immune system are crucial in mediating renal injury, yet the underlying mechanism remains unclear. In the previous studies, we found that LIGHT and its receptors HVEM/LTβR were remarkably increased in mice with IRI. In contrast, renal injury was dramatically decreased in LIGHT gene knock-out mice, compared to the wild-type (WT) mice. We therefore hypothesized that LIGHT pathway may play a vital role in renal IRI. In the present studies, we will define the underlying mechanisms of LIGHT pathway in renal IRI in vivo and in vitro experiments, and then further explore the improvements conferred by blocking this pathway. Anticipative results will deep our knowledge for the pathophysiology mechanisms of renal IRI, which ultimately pave the way for novel treatment strategies for this clinic disease.