Abstract
Here, we reported the effects of 17beta-estradiol (E2), isoflavone genistein (Gen), and daidzein (Dai) on the production of interferon (IFN)-gamma by splenocytes isolated from C57BL/6N mice. When mouse splenocytes were stimulated with lipopolysaccharide, E2, Gen, and Dai suppressed the production of IFN-gamma. However, when only nonadherent cell populations of splenocytes were tested, none of these estrogenic compounds suppressed IFN-gamma production. This result indicates that IFN-gamma production by nonadherent cell populations of splenocytes treated with estrogens is regulated by adherent cell populations. Moreover, direct cell-cell interaction between both populations was necessary for suppression of IFN-gamma production by nonadherent populations. In addition, E2 conjugated with bovine serum albumin inhibited IFN-gamma production as well as E2. This result suggests that the plasma membrane-associated estrogen receptor plays a prominent role in this suppression mechanism.
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