Cited by 208T-cell and B-cell ImmunologyPsoriasis: Treatment and PathogenesisWnt/β-catenin signaling in development and cancer

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T cell factor 1 initiates the T helper type 2 fate by inducing the transcription factor GATA-3 and repressing interferon-γ

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Yu, Qing, Sharma, Archna, Oh, Sun Young, Moon, Hyung-Geun, Hossain, M Zulfiquer, Salay, Theresa M, Leeds, Karen E, Du, Hansen, Wu, Beibei, Waterman, Marian L, Zhu, Zhou, Sen, Jyoti Misra·2009·Nature Immunology

DOI 10.1038/ni.1762PMC PMC2824257

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Abstract

The differentiation of activated CD4(+) T cells into the T helper type 1 (T(H)1) or T(H)2 fate is regulated by cytokines and the transcription factors T-bet and GATA-3. Whereas interleukin 12 (IL-12) produced by antigen-presenting cells initiates the T(H)1 fate, signals that initiate the T(H)2 fate are not completely characterized. Here we show that early GATA-3 expression, required for T(H)2 differentiation, was induced by T cell factor 1 (TCF-1) and its cofactor beta-catenin, mainly from the proximal Gata3 promoter upstream of exon 1b. This activity was induced after T cell antigen receptor (TCR) stimulation and was independent of IL-4 receptor signaling through the transcription factor STAT6. Furthermore, TCF-1 blocked T(H)1 fate by negatively regulating interferon-gamma (IFN-gamma) expression independently of beta-catenin. Thus, TCF-1 initiates T(H)2 differentiation of activated CD4(+) T cells by promoting GATA-3 expression and suppressing IFN-gamma expression.

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Authors: Yu, Q., Sharma, A., Oh, S. Y., Moon, H.-G., Hossain, M. Z., Salay, T. M., Leeds, K. E., Du, H., Wu, B., Waterman, M. L., Zhu, Z., & Sen, J. M.
Affiliations: National Institutes of Health (US)
Johns Hopkins University (US)
University of California, Irvine (US)
Corresponding author: Sen, Jyoti Misra
ORCID: Yu, Qing
Sharma, Archna
Oh, Sun Young
Moon, Hyung-Geun
Wu, Beibei
Waterman, Marian L
Zhu, Zhou
Sen, Jyoti Misra
Venue: Nature Immunology
Publisher: Springer Science and Business Media LLC
Published: 2009-08-02
Volume: 10
Issue: 9
Pages: 992-999
ISSN: 1529-2908 (ISSN-L)
1529-2916
DOI: 10.1038/ni.1762
PMC: PMC2824257
OpenAlex: W2007359758
Cited by: 208
References: 50
Citations by year: 2026: 5 · 2025: 5 · 2024: 11 · 2023: 4 · 2022: 10 · 2021: 16 · 2020: 12 · 2019: 11 · 2018: 10 · 2017: 12 · 2016: 16 · 2015: 20 · 2014: 13 · 2013: 14 · 2012: 15
FWCI: 7.05
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
Locations: Nature Immunology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: Canadian Institute for Theoretical Astrophysics
National Institutes of Health
National Institute on Aging (Z01AG000772)
Topics: Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Wnt/β-catenin signaling in development and cancer
Keywords: TCF1, GATA3, T cell receptor signaling, β-catenin, CD4+ T cell polarization, STAT6, T-bet
MeSH terms: Animals, Cell Differentiation, Interferon-gamma, Mice, Inbred C57BL, Promoter Regions, Genetic, Receptors, Antigen, T-Cell, Interleukin-4, Th2 Cells, Interleukin-12, GATA3 Transcription Factor, beta Catenin, Mice, T Cell Transcription Factor 1, Receptors, Notch

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T cell factor 1 initiates the T helper type 2 fate by inducing the transcription factor GATA-3 and repressing interferon-γ

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