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Cited by 518Asthma and respiratory diseasesT-cell and B-cell ImmunologyNF-κB Signaling Pathways

A critical role for NF-κB in Gata3 expression and TH2 differentiation in allergic airway inflammation

Das, Jyoti, Chen, Chang-Hung, Yang, Liyan, Cohn, Lauren, Ray, Prabir, Ray, Anuradha·2001·Nature Immunology
DOI 10.1038/83158
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Abstract

The transcription factor GATA-3 is expressed in T helper 2 (TH2) but not TH1 cells and plays a critical role in TH2 differentiation and allergic airway inflammation in vivo. Mice that lack the p50 subunit of nuclear factor kappa B (NF-kappa B) are unable to mount airway eosinophilic inflammation. We show here that this is not due to defects in TH2 cell recruitment but due to the inability of the p50-/- mice to produce interleukin 4 (IL-4), IL-5 and IL-13: cytokines that play distinct roles in asthma pathogenesis. CD4+ T cells from p50-/- mice failed to induce Gata3 expression under TH2-differentiating conditions but showed unimpaired T-bet expression and interferon gamma (IFN-gamma) production under TH1-differentiating conditions. Inhibition of NF-kappa B activity prevented GATA-3 expression and TH2 cytokine production in developing, but not committed, TH2 cells. Our studies provide a molecular basis for the need for both T cell receptor and cytokine signaling for GATA-3 expression and, in turn, TH2 differentiation.

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  • M2 depletion caused an increase in the number and proportion of iNOS+ M1 cells.

    “M2 depletion caused an increase in the number and proportion of iNOS+ M1 cells (Fig. 5d and Supplementary Fig. 8g online), supporting previous findings of reciprocal regulation between M1 and M2 polarization and associated cytokines25, 26.”

    From M2 microglia and macrophages drive oligodendrocyte differentiation during CNS remyelination (2013) · cites this paper as [25]

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Authors
Das, J., Chen, C.-H., Yang, L., Cohn, L., Ray, P., & Ray, A.
Affiliations
Yale University (US)
Corresponding author
Ray, Anuradha
ORCID
Venue
Nature Immunology
Publisher
Springer Science and Business Media LLC
Published
2001-01
Volume
2
Issue
1
Pages
45-50
ISSN
  • 1529-2908 (ISSN-L)
  • 1529-2916
DOI
10.1038/83158
OpenAlex
W1555985183
Cited by
518
References
42
Citations by year
2026: 10 · 2025: 16 · 2024: 11 · 2023: 13 · 2022: 14 · 2021: 12 · 2020: 20 · 2019: 13 · 2018: 16 · 2017: 21 · 2016: 15 · 2015: 12 · 2014: 17 · 2013: 18 · 2012: 29
FWCI
22.92
Type
journal article
Language
en
Open access
closed
Licence
www.springer.com/tdm (tdm)
Locations
  • Nature Immunology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords
NF-κB, GATA3, Th2 differentiation, allergic airway inflammation, asthma, p50 subunit, IL-4, IL-5, IL-13, CD4+ T cells, T-bet, interferon-gamma, T cell receptor signaling, cytokine signaling, eosinophilic inflammation
MeSH terms
Animals, Asthma, Cell Differentiation, Disease Models, Animal, DNA-Binding Proteins, Signal Transduction, Trans-Activators, Gene Expression, NF-kappa B, Mice, Knockout, Th1 Cells, Th2 Cells, STAT6 Transcription Factor, GATA3 Transcription Factor, Mice, NF-kappa B p50 Subunit

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