17β-ESTRODIOL DIFFERENTLY MODULATES DC FROM MURINE BONE MARROW AND SPLEEN
Estrogen has been known very important to control immune reaction, especially in autoimmune disease. Dendritic cells (DCs) are the most powerful antigerrpresenting cells to initiate immune response. Our purpose was to find out the effect of estrogen on DCs of various sources and maturation phases in BALB/c female mice. Our result showed that 17β - estrodiol (E2) promoted bone marrow precursors to differentiate into CD11c+ DCs. E2 enhanced bone marrow derived immature DCs, mature DCs and spleen DCs to express surface molecules CD40, CD80, CD86, and promote their stimulation function. E2 also promoted the marrow immature DCs to produce cytokines IL - 6, IL - 10, IL - 12 and TNFα, but decreased them in the marrow mature DCs and spleen DCs. ERα mRNA expression in spleen DCs could be increased by E2. Tamoxifen antagonized E2 effect on DCs. These data suggested that E2 dissimilarly controlled the differentiation, maturation and functions of different subsets of DCs. These may were achieved through E2 binding ER to modulate target gene transcription.
17β - estrodiol dendritic cells bone marrow spleen BALB/c mice
Bo Jiang Lingyun Sun Xiaoxi Li Sha Hao Yayi Hou
Immunology and Reproductive Biology Lab, Medical School and State Key Laboratory of Pharmaceutical B Rheumatology and Immunology department, The Affiliated Drum Tower Hospital of Nanjing University Med Immunology and Reproductive Biology Lab, Medical School and State Key Laboratory of Pharmaceutical B
国际会议
The 4th International Forum on Post-genome Technologies(4IFPT)(第四届国际后基因组生命科学技术学术论坛)
杭州
英文
412-415
2006-09-25（万方平台首次上网日期，不代表论文的发表时间）