Interleukin (IL)-6 Directs the Differentiation of IL-4–producing CD4+ T Cells

DOI PDF 被引用文献30件
  • Mercedes Rincón
    From the *Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520-8011; ‡Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-9031; and §Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06520-8011
  • Juan Anguita
    From the *Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520-8011; ‡Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-9031; and §Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06520-8011
  • Tetsuo Nakamura
    From the *Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520-8011; ‡Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-9031; and §Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06520-8011
  • Erol Fikrig
    From the *Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520-8011; ‡Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-9031; and §Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06520-8011
  • Richard A. Flavell
    From the *Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520-8011; ‡Section of Rheumatology, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-9031; and §Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06520-8011

書誌事項

公開日
1997-02-03
DOI
  • 10.1084/jem.185.3.461
公開者
Rockefeller University Press

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説明

<jats:p>Interleukin (IL)-4 is the most potent factor that causes naive CD4+ T cells to differentiate to the T helper cell (Th) 2 phenotype, while IL-12 and interferon γ trigger the differentiation of Th1 cells. However, the source of the initial polarizing IL-4 remains unclear. Here, we show that IL-6, probably secreted by antigen-presenting cells, is able to polarize naive CD4+ T cells to effector Th2 cells by inducing the initial production of IL-4 in CD4+ T cells. These results show that the nature of the cytokine (IL-12 or IL-6), which is produced by antigen-presenting cells in response to a particular pathogen, is a key factor in determining the nature of the immune response.</jats:p>

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