Skip NavigationSkip to Content

IL-7 receptor signals inhibit expression of transcription factors TCF-1, LEF-1, and ROR gamma t: Impact on thymocyte development

  1. Author:
    Yu, Q.
    Erman, B.
    Park, J. H.
    Feigenbaum, L.
    Singer, A.
  2. Author Address

    NCI, Expt Immunol Branch, NIH, Bethesda, MD 20892 USA. NCI, SAIC Frederick, Frederick Canc Res & Dev Ctr, Frederick, MD 21702 USA Singer, A, NCI, Expt Immunol Branch, NIH, Bldg 10,Rm 4B36, Bethesda, MD 20892 USA
    1. Year: 2004
    2. Date: SEP 20
  1. Journal: Journal of Experimental Medicine
    1. 200
    2. 6
    3. Pages: 797-803
  2. Type of Article: Article
  1. Abstract:

    Intrathymic T cell development depends on signals transduced by both T cell receptor and cytokine receptors. Early CD4(-)CD8(-) (double negative) thymocytes require interleukin (IL)-7 receptor (IL-7R) signals for survival and proliferation, but IL-7R signals are normally extinguished by the immature single positive (ISP) stage of thymocyte development. We now demonstrate that IL-7R signals inhibit expression of transcription factors TCF-1, LEF-1, and ROR-gammat that are required for the ISP to double positive (DP) transition in the thymus. In addition, we demonstrate that IL-7R signals also inhibit TCF-1 and LEF-1 expression in mature peripheral T cells. Thus, the present work has identified several important downstream target genes of IL-7R signaling in T cells and thymocytes that provide a molecular mechanism for the inhibitory influence of IL-7R signaling on DP thymocyte development. We conclude that IL-7R signals down-regulate transcription factors required for the ISP to DP transition and so must be terminated by the ISP stage of thymocyte development

    See More

External Sources

  1. WOS: 000224105500010

Library Notes

  1. No notes added.
NCI at Frederick

You are leaving a government website.

This external link provides additional information that is consistent with the intended purpose of this site. The government cannot attest to the accuracy of a non-federal site.

Linking to a non-federal site does not constitute an endorsement by this institution or any of its employees of the sponsors or the information and products presented on the site. You will be subject to the destination site's privacy policy when you follow the link.

ContinueCancel