Article abstract


Nature Immunology 9, 1122 - 1130 (2008)
Published online: 7 September 2008 | doi:10.1038/ni.1647

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

Lie Wang1, Kathryn F Wildt1, Jinfang Zhu2, Xianyu Zhang3, Lionel Feigenbaum4, Lino Tessarollo5, William E Paul2, B J Fowlkes3 & Rémy Bosselut1


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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  1. Laboratory of Immune Cell Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
  2. Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
  3. Laboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
  4. National Cancer Institute–Science Applications International Corporation, Frederick, Maryland 21702, USA.
  5. Mouse Cancer Genetics Program, Center for Cancer Research, National Cancer Institute, Frederick, Maryland 21702, USA.

Correspondence to: Rémy Bosselut1 e-mail: remy@helix.nih.gov



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