Stat5a regulates T helper cell differentiation by several distinct mechanisms

DOI PDF 被引用文献8件
  • Shin-ichiro Kagami
    From the Department of Internal Medicine II, Chiba University School of Medicine, Japan; Department of Hematopoietic Factors, The Institute of Medical Science, University of Tokyo, Japan; and Takara Shuzo, Biotechnology Research Laboratories, Shiga, Japan.
  • Hiroshi Nakajima
    From the Department of Internal Medicine II, Chiba University School of Medicine, Japan; Department of Hematopoietic Factors, The Institute of Medical Science, University of Tokyo, Japan; and Takara Shuzo, Biotechnology Research Laboratories, Shiga, Japan.
  • Akira Suto
    From the Department of Internal Medicine II, Chiba University School of Medicine, Japan; Department of Hematopoietic Factors, The Institute of Medical Science, University of Tokyo, Japan; and Takara Shuzo, Biotechnology Research Laboratories, Shiga, Japan.
  • Koichi Hirose
    From the Department of Internal Medicine II, Chiba University School of Medicine, Japan; Department of Hematopoietic Factors, The Institute of Medical Science, University of Tokyo, Japan; and Takara Shuzo, Biotechnology Research Laboratories, Shiga, Japan.
  • Kotaro Suzuki
    From the Department of Internal Medicine II, Chiba University School of Medicine, Japan; Department of Hematopoietic Factors, The Institute of Medical Science, University of Tokyo, Japan; and Takara Shuzo, Biotechnology Research Laboratories, Shiga, Japan.
  • Sumiyo Morita
    From the Department of Internal Medicine II, Chiba University School of Medicine, Japan; Department of Hematopoietic Factors, The Institute of Medical Science, University of Tokyo, Japan; and Takara Shuzo, Biotechnology Research Laboratories, Shiga, Japan.
  • Ikunoshin Kato
    From the Department of Internal Medicine II, Chiba University School of Medicine, Japan; Department of Hematopoietic Factors, The Institute of Medical Science, University of Tokyo, Japan; and Takara Shuzo, Biotechnology Research Laboratories, Shiga, Japan.
  • Yasushi Saito
    From the Department of Internal Medicine II, Chiba University School of Medicine, Japan; Department of Hematopoietic Factors, The Institute of Medical Science, University of Tokyo, Japan; and Takara Shuzo, Biotechnology Research Laboratories, Shiga, Japan.
  • Toshio Kitamura
    From the Department of Internal Medicine II, Chiba University School of Medicine, Japan; Department of Hematopoietic Factors, The Institute of Medical Science, University of Tokyo, Japan; and Takara Shuzo, Biotechnology Research Laboratories, Shiga, Japan.
  • Itsuo Iwamoto
    From the Department of Internal Medicine II, Chiba University School of Medicine, Japan; Department of Hematopoietic Factors, The Institute of Medical Science, University of Tokyo, Japan; and Takara Shuzo, Biotechnology Research Laboratories, Shiga, Japan.

この論文をさがす

抄録

<jats:title>Abstract</jats:title><jats:p>We have previously shown that CD4+ T cell–mediated allergic inflammation is diminished in signal transducer and activator of transcription (Stat)5a-deficient (Stat5a−/−) mice. To determine whether Stat5a regulates T helper cell differentiation, we studied T helper (Th)1 and Th2 cell differentiation of Stat5a−/−CD4+ T cells at single-cell levels. First, Th2 cell differentiation from antigen-stimulated splenocytes was significantly decreased in Stat5a−/− mice as compared with that in wild-type mice. Further, Th2 cell differentiation was also impaired in Stat5a−/− mice even when purified CD4+ T cells were stimulated with anti-CD3 plus anti-CD28 antibodies in the presence of interleukin-4. Moreover, the retrovirus-mediated gene expression of Stat5a in Stat5a−/−CD4+ T cells restored the Th2 cell differentiation at the similar levels to that in wild-type CD4+ T cells. In addition, interleukin-4 normally phosphorylated Stat6 in CD4+ T cells from Stat5a−/− mice. Second, the development of CD4+CD25+ immunoregulatory T cells was impaired in Stat5a−/− mice, as indicated by a significant decrease in the number of CD4+CD25+ T cells in Stat5a−/− mice. Furthermore, the depletion of CD4+CD25+ T cells from wild-type splenocytes significantly decreased Th2 cell differentiation but increased Th1 cell differentiation, whereas the depletion of CD4+CD25+ T cells from Stat5a−/−splenocytes had no significant effect on the Th1 and Th2 cell differentiation. Together, these results indicate that the intrinsic expression of Stat5a in CD4+ T cells is required for Th2 cell differentiation and that Stat5a is involved in the development of CD4+CD25+ immunoregulatory T cells that modulate T helper cell differentiation toward Th2 cells.</jats:p>

収録刊行物

  • Blood

    Blood 97 (8), 2358-2365, 2001-04-15

    American Society of Hematology

被引用文献 (8)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ