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

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Late Developmental Plasticity in the T Helper 17 Lineage

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Lee, Yun Kyung, Turner, Henrietta, Maynard, Craig L., Oliver, James R., Chen, Dongquan, Elson, Charles O., Weaver, Casey T.·2009·Immunity

DOI 10.1016/j.immuni.2008.11.005PMC PMC3607320

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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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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.
ORCID: Lee, Yun Kyung
Maynard, Craig L.
Chen, Dongquan
Elson, Charles O.
Weaver, Casey T.
Venue: Immunity
Publisher: Elsevier BV
Published: 2009-01
Volume: 30
Issue: 1
Pages: 92-107
ISSN: 1074-7613 (ISSN-L)
DOI: 10.1016/j.immuni.2008.11.005
PMC: PMC3607320
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: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 1694 d)
doi.org/10.15223/policy-017 (stm-asf)
doi.org/10.15223/policy-037 (stm-asf)
doi.org/10.15223/policy-012 (stm-asf)
doi.org/10.15223/policy-029 (stm-asf)
doi.org/10.15223/policy-004 (stm-asf)
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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Late Developmental Plasticity in the T Helper 17 Lineage

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