Cited by 1,053Psoriasis: Treatment and PathogenesisT-cell and B-cell ImmunologyCytokine Signaling Pathways and Interactions

The DOI matches its Crossref record; 62 of the 62 references it cites were found in a registry or an index.

Late Developmental Plasticity in the T Helper 17 Lineage

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Abstract

Development of T helper (Th) 17 cells requires transforming growth factor (TGF)-beta and interleukin (IL)-6 and is independent of the Th1 pathway. Although T cells that produce interferon (IFN)-gamma are a recognized feature of Th17 cell responses, mice deficient for STAT4 and T-bet-two prototypical Th1 transcription factors-are protected from autoimmunity associated with Th17 pathogenesis. To examine the fate and pathogenic potential of Th17 cells and origin of IFN-gamma-producing T cells that emerge during Th17 immunity, we developed IL-17F reporter mice that identify cells committed to expression of IL-17F and IL-17A. Th17 cells required TGF-beta for sustained expression of IL-17F and IL-17A. In the absence of TGF-beta, both IL-23 and IL-12 acted to suppress IL-17 and enhance IFN-gamma production in a STAT4- and T-bet-dependent manner, albeit with distinct efficiencies. These results support a model of late Th17 developmental plasticity with implications for autoimmunity and host defense.

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Crossref · 10.1016/j.immuni.2008.11.005

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Metadata

Authors
Lee, Y. K., Turner, H., Maynard, C. L., Oliver, J. R., Chen, D., Elson, C. O., & Weaver, C. T.
Affiliations
University of Alabama at Birmingham (US)
Corresponding author
Weaver, Casey T.
Venue
Immunity
Publisher
Elsevier BV
Published
2009-01
Volume
30
Issue
1
Pages
92-107
ISSN
1074-7613 (ISSN-L)
OpenAlex
W2011882192
Cited by
1,053
References
62
Citations by year
2026: 19 · 2025: 23 · 2024: 18 · 2023: 32 · 2022: 47 · 2021: 42 · 2020: 47 · 2019: 46 · 2018: 35 · 2017: 56 · 2016: 48 · 2015: 82 · 2014: 81 · 2013: 85 · 2012: 90
FWCI
56.09
Type
journal article
Language
en
Open access
Locations
  • Immunity (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institutes of Health
  • Comprehensive Cancer Center, University of Alabama at Birmingham
  • National Institute of Allergy and Infectious Diseases (R01AI077574, R01AI035783)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R24DK064400, P01DK071176)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
Keywords
Th17 cells, T helper cell differentiation, developmental plasticity, TGF-beta, interleukin-6, IL-17F, IL-17A, interferon-gamma, STAT4, T-bet, IL-23, IL-12, autoimmunity, Th1 cells
MeSH terms
Animals, Cells, Cultured, Flow Cytometry, Interferon-gamma, T-Lymphocyte Subsets, Transforming Growth Factor beta, Mice, Knockout, Th1 Cells, Th2 Cells, Cell Lineage, Interleukin-17, Mice, Interleukin-23

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