IgM production of lymphocytes from C57BL/6N mice was stimulated by estrogen treated splenic adherent cells.

Estrogens have diverse effects on cell growth, differentiation and homeostatic functions, and have been shown to play an important role in regulating immune system. In this study, we examined the effect of 17beta-estradiol (E2) on antibody production by splenocytes isolated from C57BL/6N mice. Our results suggest that the activation of immunoglobulin (Ig) M production by E2 requires direct cell-cell interaction between adherent and non-adherent cells in mouse splenocyte population, and the primary target of E2 is adherent cell population. In addition, we indicated that ER antagonist ICI 182780 suppressed this enhancing effect of E2. Both ERalpha agonist and ERalpha agonist enhanced IgM production of mouse splenocytes. ERs are expressed on plasma membrane as well as in nucleus. However, a plasma membrane-associated ER specific ligand has no stimulation effect on IgM production. In conclusion, our results indicate that adherent cells stimulated by E2 up-regulate IgM production of lymphocytes through the direct cell-cell interactions, and the enhancing effect of E2 is arouse through ERalpha and ERbeta on these cells.