Mako Nakaya, Hirofumi Tachibana and Koji Yamada
Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University, 6-10-1 Hakozaki, Higashi-ku, Fukuoka 812-8581, Japan
Abstract: Estrogens have diverse effects on cell growth, differentiation and homeostatic functions, and have been shown to play an important role in regulating immune system. Most of these E2 functions are mediated by estrogen receptors (ERs). Recently, it was reported that ERs were expressed immunocompetent cells, such as B cell, T cell, Natural killer cell and macrophage. In this study, it was examined that effect of 17 ß-Estradiol (E2) on antibody production by splenocytes isolated from C57BL/6N mice. E2 regulates immunoglobulin M (IgM) production by mouse splenocytes. IgM production was enhanced 2.0-fold at 10-10 M E2. This enhancing effect of E2 was canceled by ER antagonist ICI 182780. Previously, it was reported that two subtypes of ERs, such as ERa and ERß. Both ERa selective agonist, 4,4',4"-(4-propyl- [1H]-prazole-1, 3, 5-triyl)trisphenol and ERß selective agonist, 2,3-bis-(4-hydroxyphenyl)-propionitrile enhanced the production of IgM as well as E2. Recently, ERs are expressed in plasma membrane as well as in nucleus. E2 conjugated to bovine serum albumin (E2-BSA) is a plasma membrane-associated ER specific ligand. E2-BSA has no effects on IgM production by mouse splenocytes. In conclusion, our results indicate that E2 up-regulates the production of IgM through interaction with ERa and ERß by mouse splenocytes. The enhancing effect of E2 was not induced by plasma membrane-associated ER.
Key words: 17ß-estradiol; splenocytes; immunoglobulin M; estrogen receptor.
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