Cited by 285T-cell and B-cell ImmunologyPsoriasis: Treatment and PathogenesisCytokine Signaling Pathways and Interactions

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Independent roles for IL-2 and GATA-3 in stimulating naive CD4+ T cells to generate a Th2-inducing cytokine environment

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Yamane, Hidehiro, Zhu, Jinfang, Paul, William E.·2005·The Journal of Experimental Medicine

DOI 10.1084/jem.20051304PMC PMC2212937

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Abstract

T cell receptor (TCR) signaling plays an important role in early interleukin (IL)-4 production by naive CD4+ T cells. This "antigen-stimulated" early IL-4 is sufficient for in vitro Th2 differentiation. Here, we provide evidence that early IL-4 production by naive CD4+ T cells stimulated with cognate peptide requires TCR-induced early GATA-3 expression and IL-2 receptor signaling, both of which are controlled by the degree of activation of extracellular signal-regulated kinase (ERK). Stimulation of naive CD4+ T cells from TCR transgenic mice with low concentrations of peptide-induced IL-2-dependent STAT5 phosphorylation, IL-4-independent early GATA-3 expression, and IL-4 production. Neutralization of IL-2 abolished early IL-4 production without affecting early GATA-3 expression. In addition, naive CD4+ T cells from GATA-3 conditional KO mice failed to produce early IL-4 in response to TCR/CD28 stimulation. Stimulation with high concentrations of peptide abrogated early GATA-3 expression and IL-2-dependent STAT5 phosphorylation, and resulted in the failure to produce early IL-4. This high concentration-mediated suppression of early IL-4 production was reversed by blockade of the ERK pathway. A MEK inhibition rescued early GATA-3 expression and responsiveness to IL-2; these cells were now capable of producing early IL-4 and undergoing subsequent Th2 differentiation.

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Authors: Yamane, H., Zhu, J., & Paul, W. E.
Affiliations: National Institutes of Health (US)
ORCID: Yamane, Hidehiro
Zhu, Jinfang
Venue: The Journal of Experimental Medicine
Publisher: Rockefeller University Press
Published: 2005-09-19
Volume: 202
Issue: 6
Pages: 793-804
ISSN: 0022-1007 (ISSN-L)
1540-9538
DOI: 10.1084/jem.20051304
PMC: PMC2212937
OpenAlex: W2128181270
Cited by: 285
References: 38
Citations by year: 2026: 3 · 2025: 7 · 2024: 10 · 2023: 11 · 2022: 11 · 2021: 15 · 2020: 8 · 2019: 10 · 2018: 13 · 2017: 18 · 2016: 13 · 2015: 18 · 2014: 28 · 2013: 16 · 2012: 19
FWCI: 3.91
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: The Journal of Experimental Medicine (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion, cc-by-nc-sa)
PubMed (publishedVersion)
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 › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
Keywords: interleukin-2, GATA3, naive CD4+ T cells, Th2 differentiation, IL-4 production, T cell receptor signaling, ERK signaling, STAT5 phosphorylation, MEK inhibition, CD28 costimulation, TCR transgenic mice, cytokine environment
MeSH terms: Animals, Butadienes, Cells, Cultured, Dendritic Cells, DNA-Binding Proteins, Fluoresceins, Interferon-gamma, Interleukin-2, Lymphocyte Activation, Mice, Inbred A, Mice, Inbred C57BL, Mice, Transgenic, Milk Proteins, Nitriles, Peptides, Phosphorylation, RNA, Messenger, Succinimides, CD4-Positive T-Lymphocytes, Trans-Activators, Interleukin-4, Cytokines, Mice, Knockout, Th2 Cells, Coculture Techniques, MAP Kinase Kinase Kinases, STAT5 Transcription Factor, GATA3 Transcription Factor, Mice

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Independent roles for IL-2 and GATA-3 in stimulating naive CD4+ T cells to generate a Th2-inducing cytokine environment

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