17BETA-ESTRADIOL REGULATES IMMUNOGLOBULIN M PRODUCTION THROUGH INTERACTION WITH ESTROGEN RECEPTORS

摘要

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 wasreported 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 beta-Estradiol (E2) on antibody production by splenocytes isolated from C57BL/6N mice. E2regulates 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 asER alpha and ER beta. Both ERa selective agonist, 4,4',4"-(4-propyl-[1H]-prazole-1, 3, 5-triyl)trisphenol and ER beta selective agonist, 2,3-bis-(4-hydroxyphenyl)-propionitrile enhanced the production of IgM as well as E2. Recently, ERs are expressed inplasma 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 ERp by mouse splenocytes. The enhancing effect of E2 was not induced by plasma membrane-associated ER.