Estrogenic compounds suppressed interferon-gamma production in mouse splenocytes through direct cell-cell interaction

Mako Nakaya, Masao Yamasaki, Yoshiyuki Miyazaki, Hirofumi Tachibana, Koji Yamada

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

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

Original languageEnglish
Pages (from-to)383-387
Number of pages5
JournalIn Vitro Cellular and Developmental Biology - Animal
Volume39
Issue number8-9
Publication statusPublished - Sep 2003

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Cell Communication
Interferons
Interferon-gamma
Estrogens
Genistein
Population
Cells
Isoflavones
Bovine Serum Albumin
Inbred C57BL Mouse
Estrogen Receptors
Lipopolysaccharides
Cell membranes
Estradiol
Cell Membrane
daidzein

All Science Journal Classification (ASJC) codes

  • Developmental Biology
  • Clinical Biochemistry
  • Cell Biology

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Estrogenic compounds suppressed interferon-gamma production in mouse splenocytes through direct cell-cell interaction. / Nakaya, Mako; Yamasaki, Masao; Miyazaki, Yoshiyuki; Tachibana, Hirofumi; Yamada, Koji.

In: In Vitro Cellular and Developmental Biology - Animal, Vol. 39, No. 8-9, 09.2003, p. 383-387.

Research output: Contribution to journalArticle

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