17β-estradiol enhances the response of plasmacytoid dendritic cell to cpg17β-estradiol提高响应的血浆cpg树突细胞.pdf

17b-Estradiol Enhances the Response of Plasmacytoid Dendritic Cell to CpG 1 1 1 2 3 1,4 Xiaoxi Li , Yixin Xu , Ling Ma , Lingyun Sun , Gengfeng Fu , Yayi Hou * 1 Immunology and Reproductive Biology Lab, Medical School and State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, Jiangsu, People’s Republic of China, 2 Drum Tower Hospital, Nanjing University Medical School, Nanjing, Jiangsu, People’s Republic of China, 3 Jiangsu Centers for Diseases Prevention and Control, Jiangsu, People’s Republic of China, 4 Jiangsu Key Laboratory of Molecular Medicine, Nanjing, Jiangsu, People’s Republic of China Abstract Gender differences in immune capabilities suggest that sex hormones such as estrogens were involved in the regulation of the immunocompetence. Numerous studies also suggest that plasmacytoid dendritic cells (PDCs) play a pathogenic role in SLE. However, it is unclear whether estrogen can modulate the function of PDCs to influence the development of SLE. In the present study, PDCs from murine spleens were treated with 17b-estradiol (E2) and CpG respectively or both in vitro, then cell viability, costimulatory molecule expression, cytokine secretion of PDCs, as well as stimulatory capacity of PDCs to B cells were analyzed. Results showed that E2 and CpG increased the cell viability and costimulatory molecule expression on PDCs synergistically. Moreover, the intracellular and extracellular secretion of IFN-a was increased by E2 or E2 plus CpG. In addition, E2 and CpG also increased the stimulatory capacity of PDCs to B cells, and the viability of B cells was decreased after neutralizing IFN-a significantly. In the experiments in vivo, mice received daily s.c. injections of E2 and CpG respecti