血管通透性增加是肾综合征出血热（HFRS）的基本病理改变之一，文献表明炎症因子引起的免疫病理损伤可能参与致病机制，但其作用的关键因子仍不明确。CD100是一种白细胞分化抗原，主要表达于T淋巴细胞，可由金属蛋白酶裂解后产生可溶型CD100（sCD100），膜型CD100和sCD100均具有生物学活性，与其受体PlexinB1结合可以激活RhoA，而RhoA是引起血管内皮细胞通透性升高的重要信号分子。我们最近研究发现，HFRS患者急性期血浆sCD100水平显著升高与病情相关，并对血浆高水平sCD100的产生机制及其在内皮细胞通透性增加中的作用进行了初步探讨。本项目拟在前期研究基础上，深入研究sCD100产生的机制，明确sCD100使内皮细胞通透性增加的分子机制，阐明sCD100在HFRS病理损伤中的作用。这些研究能拓展对HFRS病理损伤机制的认识，为临床治疗HFRS的新靶点提供理论和实验依据。

One of the basic pathological characteristics of hemorrhagic fever with renal syndrome(HFRS) is the hyperpermeability of vascular endothelial cell. Many articles reported that immunopathogenesis caused by the inflammatory factors be involved in the pathomechanism of HFRS, but the key factors remain unclear. CD100, a menber of the leucocyte differentiation antigens, is dominantly expressed in T lymphocyte. The soluble form CD100 is released from the cell surface after splitted by metalloproteases. Both the membrane-bound and soluble CD100 are biologic active. By binding to PlexinB1, CD100 can active RhoA which is one of the important molecules related to the hyperpermeability of the vascular endothelial cell（VEC）. A recent study on the sCD100 in the plasma of the HFRS patients showed that sCD100 increased significantly and changed corresponding to the patients' condition. Then we investigate the source of the sCD100 and it's role in the pathomechanism initially. Here we'll lucubrate the phenomenon and pathomechanism correlated with sCD100 , which may increase our knowledge of the pathomechanism of HFRS and may support new targets to prevent and cure the HFRS with theory and experiment data.