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Distinct functions for the transcription factors GATA-3 and ThPOK during intrathymic differentiation of CD4(+) T cells

  1. Author:
    Wang, L.
    Wildt, K. F.
    Zhu, J. F.
    Zhang, X. Y.
    Feigenbaum, L.
    Tessarollo, L.
    Paul, W. E.
    Fowlkes, B. J.
    Bosselut, R.

  2. Author Address

    Wang, Lie, Wildt, Kathryn F.; Bosselut, Remy] NCI, Lab Immune Cell Biol, Ctr Canc Res, NIH, Bethesda, MD 20892 USA. [Zhu, Jinfang, Paul, William E.] NIAID, Immunol Lab, NIH, Bethesda, MD 20892 USA. [Zhang, Xianyu, Fowlkes, B. J.] NIAID, Cellular & Mol Immunol Lab, NIH, Bethesda, MD 20892 USA. [Feigenbaum, Lionel] NCI, Sci Applicat Int Corp, Frederick, MD 21702 USA. [Tessarollo, Lino] NCI, Mouse Canc Genet Program, Ctr Canc Res, Frederick, MD 21702 USA.
    1. Year: 2008
  2. Journal: Nature Immunology
    1. 9
    2. 10
    3. Pages: 1122-1130
  4. Type of Article: Article
  1. Abstract:

    The transcription factors GATA-3 and ThPOK are required for intrathymic differentiation of CD4(+) T cells, but their precise functions in this process remain unclear. Here we show that, contrary to previous findings, Gata3 disruption blocked differentiation into the CD4(+) T cell lineage before commitment to the CD4(+) lineage and in some contexts permitted the 'redirection' of major histocompatibility complex class II-restricted thymocytes into the CD8(+) lineage. GATA-3 promoted ThPOK expression and bound to a region of the locus encoding ThPOK established as being critical for ThPOK expression. Finally, ThPOK promoted differentiation into the CD4(+) lineage in a way dependent on GATA-3 but inhibited differentiation into the CD8(+) lineage independently of GATA-3. We propose that GATA-3 acts as a specification factor for the CD4(+) lineage 'upstream' of the ThPOK-controlled CD4(+) commitment checkpoint.

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External Sources

  1. PMID: 18776904

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