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Updated: May 31, 2026

Generation of Human CD40-activated B cells
Published on: October 16, 2009
Estrogen promotes B cell activation in vitro through down-regulating CD80 molecule expression
Yibing Fu1, Li Li, Xiaowen Liu
1Key Laboratory for Reproductive Medicine of Shandong Province, Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, PR China.
Estrogen is the main female hormone of women. It has diverse effects on cell growth, differentiation and homeostatic functions. Accumulated evidence has indicated that estrogen may regulate multiple immune functions and the immune status of women. However, there is little report on the effect of estrogen on mature B cell functions. In this study, we observed the effect of 17β-estradiol (E2) on the proliferation, apoptosis, antibody production and differentiation of splenic B cells of mice in vitro. Splenocytes of female BALB/c mice were isolated and cultured with E2. E2 treatments decreased the expression of CD80 molecule on splenic B cells but enhanced the total IgG antibody production of splenocyte, without promoting the differentiation of B cells to plasma cells. E2 protected splenic B cells from the serum-deficiency-induced apoptosis but had no influence on the proliferation of B cells. These results suggest that estrogen may promote the activity of B cells through down-regulating the expression of CD80 molecule on B cells.
Estrogen is the main female hormone of women. It has diverse effects on cell growth, differentiation and homeostatic functions. Accumulated evidence has indicated that estrogen may regulate multiple immune functions and the immune status of women. However, there is little report on the effect of estrogen on mature B cell functions. In this study, we observed the effect of 17β-estradiol (E2) on the proliferation, apoptosis, antibody production and differentiation of splenic B cells of mice in vitro. Splenocytes of female BALB/c mice were isolated and cultured with E2. E2 treatments decreased the expression of CD80 molecule on splenic B cells but enhanced the total IgG antibody production of splenocyte, without promoting the differentiation of B cells to plasma cells. E2 protected splenic B cells from the serum-deficiency-induced apoptosis but had no influence on the proliferation of B cells. These results suggest that estrogen may promote the activity of B cells through down-regulating the expression of CD80 molecule on B cells.
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