慢性肾脏病（CKD）发病率逐年升高，但其免疫学机制有待全面深入研究。我们在前期研究中发现机体淋巴管一般处于休止状态，只有受损脏器才会发生淋巴管增殖。肾脏纤维化进程中伴随大量淋巴管新生，并与患者肾脏病变程度密切相关。初步敲除淋巴管，发现肾脏、淋巴结、脾脏中各种免疫细胞发生相应变化，并可改善肾脏纤维化，提示淋巴管新生可能通过调控脾肾免疫对话影响肾脏纤维化进程中免疫反应。在此基础上，本研究拟在不影响固有淋巴管功能情况下，特异性敲除肾脏新生淋巴管，探讨肾脏区域免疫特性及肾脏纤维化进程中脾肾对话机制，以及靶向该免疫调控网络，延缓肾脏纤维化的干预策略，为慢性肾脏病开辟新的治疗途径。

The incidence of chronic kidney disease (CKD) has increased gradually, while the immune mechanism mechanism remains unlear. Our previous studies found that lymphatic vessels was in quiescent state in normal tissue, while lymphangiogenesis occured in injured tissue. Lymphangiogenesis was associated with the progression of renal fibrosis and the degree of CKD lesions. Through knocking out lymphatic vessels, the activated phenotypic modulation and quantity of immune cells in injured kidney, local lymph nodes and spleen were inhibited with the mitigation of renal fibrosis, indicating that lymphangiogenesis affects renal fibrosis by regulating spleen-kidney immune dialogue. On this basis, we intend to interfere the proliferation of lymphatic endothelial cells in kidney to clear the spleen-kidney immune dialogue mechanism in renal fibrosis, and explore effective intervene strategy to ameliorate ranal fibrosis.