慢性移植物抗主病（GVHD）是异基因造血干细胞移植后导致患者致死及致残的重要原因。既往研究证实辅助性T细胞17（Th17）的持续存在促进慢性GVHD的发生和发展，但其具体机制仍未完全阐明。我们前期研究发现诱导共刺激分子（ICOS）对于Th17细胞的维持至关重要。ICOS下游的转录因子c-Maf促进Th17细胞的产生及维持。故我们提出：在慢性GVHD的发展过程中，ICOS通过c-Maf参与Th17细胞维持的假说。因此，本实验拟通过体外诱导Th17细胞及建立小鼠慢性GVHD模型，使用细胞生物学、分子生物学等方法，证实在慢性GVHD中，ICOS通过c-Maf维持Th17细胞稳定性的具体机制，为以T细胞为基础的治疗提供理论依据并服务于临床。

Chronic graft-versus-host disease (cGVHD) is still the main cause of morbidity and mortality after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Previous studies have shown that the persistence of Th17 cells promote the development of cGVHD, however, the mechanism of this persistence is still incompletely known. Our preliminary study has shown that inducible co-stimulating molecule (ICOS) is involved in Th17 maintenance in cGVHD. c-Maf, a downstream transcription factor of ICOS, promotes the generation and maintenance of Th17 cells. Hence, we posit a hypothesis that ICOS maintains stability of Th17 cells via c-Maf in cGVHD. By inducing allo-reactive Th17 cells in vitro and performing murine cGVHD model, and taking advantage of cytobiology and molecular biology, we try to address the mechanism of ICOS in maintaining Th17 stability via c-Maf in cGVHD, which will be instrumental in advanced T-cell-based therapy for cGVHD, moreover, useful for clinic.