炎性细胞浸润在肾脏纤维化的起始和进展过程中都发挥着重要的"推手"作用。近年来研究证实肾脏淋巴管生成与炎性细胞浸润密切相关，但相关研究限于描述性,淋巴管生成对肾脏纤维化进展的意义还不清楚。我们发现新生淋巴管参与肾脏炎症反应和纤维化的进展，但其中分子机制还未见报道。研究表明：CD137-CD137L的相互作用在炎症反应的维持和级联放大中发挥重要作用。我们发现肾脏淋巴管内皮细胞（LEC）表达CD137，巨噬细胞和树突状细胞表达的CD137L。我们假说:肾脏LEC通过表面的CD137与巨噬细胞和树突状细胞表达的CD137L作用促进其活化，反向信号通路同时激活促进LEC的分泌CCL21，募集炎症细胞和成纤维细胞，维持肾脏局部慢性炎症反应并促进纤维化的进展。我们将结合临床标本和转基因动物模型通过一系列实验来验证此假说，从而明确以新生淋巴管为中心调控炎性细胞活化和肾脏纤维化进展的分子机制。

Inflammatory cells infiltration plays an promoting role in the initiation and progression of renal fibrosis. Recently, descriptive studies have confirmed the newly formed lymphatic vessels in the renal interstitium closely associated with inflammatory cell infiltration, however, the value of lymphangiogenesis for renal fibrosis is unclear. We found that lymphangiogenesis participate in the progression of renal inflammation and fibrosis , but the molecular mechanisms have not been reported. Studies have shown that : CD137-CD137L interactions play a crucial role in initiating and promoting the inflammatory cascade. According to our findings that kidney lymphatic endothelial cells (LEC) express CD137, macrophages and dendritic cells expressing CD137L,we make the following assumptions : in the renal interstitium, CD137 expressed by the newly formed lymphatic vessels interacts with CD137L expressed by macrophages and dendritic cells and promote their activation. Simultaneously, the activation of the reverse signal pathway promote secretion of CCL21 by LEC. CCL21 recruit inflammatory cells and fibroblasts which maintain local chronic inflammation and promote the progress of renal fibrosis. In order to test this hypothesis, we will combine clinical specimens and transgenic animal models to perform a series of experiments, and aim to define the mechanisms how the newly formed lymphatic vessels regulate inflammatory cell activation and the progression of renal fibrosis.