系统性红斑狼疮（SLE）是一种严重危害人类健康的自身免疫性疾病，免疫系统紊乱参与SLE发病。近十年来，SLE的治疗方法没有新突破。因此深入探讨SLE发病机制及寻找新的治疗靶点成为研究热点。我们前期研究发现CD8+CXCR3+T细胞功能失调和Tfh细胞大量扩增参与SLE的发生和发展，但CD8+CXCR3+T细胞如何调控Tfh细胞功能及SLE中CD8+CXCR3+T细胞功能失调的分子机制均未见报道。我们拟在阐明CD8+CXCR3+T细胞的调控机制基础上，进一步探索此类细胞的治疗作用。课题创新点主要在于：①首次阐明CD8+CXCR3+T细胞识别和调控Tfh的分子机制；②首次探索导致SLE中CD8+CXCR3+T细胞功能损伤的分子机制；③首次探索CD8+CXCR3+T细胞治疗SLE的可能性。研究结果将从全新视角阐明SLE的免疫学新机制，为其临床治疗研究拓展新思路，具有重要的科学意义和临床研究价值。

Systemic lupus erythematosus (SLE) is an autoimmune disease, which seriously endangers human health. It is considered that immune disorder is involved in the pathogenesis of SLE. In the past ten years, the treatment method of SLE does not have any new breakthrough. Therefore, study of the pathogenesis of SLE and the new therapeutic targets, has become a hot topic in research today. In the previous study, we found that dysfunction of CD8+CXCR3+T cells and a large number of Tfh cells participate in the pathogenesis of SLE. However, the molecular mechanism of CD8+CXCR3+T cells how to regulate Tfh cells and which factor to impair the function of CD8+CXCR3+T cells in SLE have not been reported for now. We intend to clarify the regulatory mechanism of CD8+CXCR3+T cells, and further explore the role of CD8+CXCR3+T cells in the treatment of SLE. The innovations of this project are as follows: ① We first elucidate the molecular mechanism of CD8+CXCR3+T cells to recognize and regulate Tfh cells; ② We explore which factors impair the function of CD8+CXCR3+T cells in SLE for the first time; ③ We first explore the possibility of CD8+CXCR3+T cells to treat SLE. The results of this study will clarify the new immunological mechanism of SLE and develop new ideas for the clinical treatment of SLE. In conclusion, this project has important scientific significance and clinical research value.