课题组在上一个国家自然基金的支持下发现系统性红斑狼疮（systemic lupus erythematosus, SLE）患者CD4+T细胞中人内源性逆转录病毒（human endogenous retroviruses, HERVs）亚型E clone 4-1表达明显增高，且受长末端重复序列（Long terminal repeats，LTRs）甲基化水平调控。但其高表达在SLE发病中的作用尚无研究。本课题拟通过qPCR分析LTRs转录活性和病毒gag表达水平对T细胞活性的影响；通过分析自身抗体水平和LTRs转录活性的相关性；通过转染病毒env的T细胞与B细胞共孵检测抗体产生的变化；通过SLE患者血清筛选env多肽文库，探讨HERV-E clone 4-1对SLE中T细胞抑制和体液免疫亢进的影响。尝试阐明HERVs对SLE发病的作用，为治疗SLE提供新的靶点。

In our previous study supported by NSFC, we found that the mRNA expression of human endogenous retroviruses (HERVs) E clone 4-1 was upregulated in systemic lupus erythematosus (SLE) CD4+ T cells, and it was modulated by the methylation level of long terminal repeats (LTRs). However, the role of upregulated HERV-E clone 4-1 in the pathogenesis of SLE remains unknown. We plan to investigate the impact of LTRs transcriptional avtivity and the expression levels of gag on the activity of T cells by qPCR; to evaluate the relationship between the levels of antoantibodies and the LTRs transcriptional activity; to detect the antibody production via co-culture of env-transfected T cells and B cells; to screen the specific env peptide using a peptide matrix mapping methodology in order to explore the role of HERV-E clone 4-1 on T cell inhibition and antibody overproduction in SLE. Through this study, we try to clarify the pathogenesis of SLE and find a new target molecule to treat SLE.