Cited by 756Psoriasis: Treatment and PathogenesisInflammatory Bowel DiseaseT-cell and B-cell Immunology

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A protective function for interleukin 17A in T cell–mediated intestinal inflammation

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O'Connor Jr, William, Kamanaka, Masahito, Booth, Carmen J, Town, Terrence, Nakae, Susumu, Iwakura, Yoichiro, Kolls, Jay K, Flavell, Richard A·2009·Nature Immunology

DOI 10.1038/ni.1736PMC PMC2709990

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Abstract

Interleukin 23 (IL-23) and IL-17 have been linked to the pathogenesis of several chronic inflammatory disorders, including inflammatory bowel disease. Yet as an important function for IL-23 is emerging, the function of IL-17 in inflammatory bowel disease remains unclear. Here we demonstrate IL-17A-mediated protection in the CD45RBhi transfer model of colitis. An accelerated wasting disease elicited by T cells deficient in IL-17A correlated with higher expression of genes encoding T helper type 1-type cytokines in colon tissue. IL-17A also modulated T helper type 1 polarization in vitro. Furthermore, T cells deficient in the IL-17 receptor elicited an accelerated, aggressive wasting disease relative to that elicited by wild-type T cells in recipient mice. Our data demonstrate a protective function for IL-17 and identify T cells as not only the source but also a target of IL-17 in vivo.

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Authors: O'Connor Jr, W., Kamanaka, M., Booth, C. J., Town, T., Nakae, S., Iwakura, Y., Kolls, J. K., & Flavell, R. A.
Affiliations: Yale University (US)
Cedars-Sinai Medical Center (US)
Institute of Medical Science, The University of Tokyo (JP)
Children's Hospital of Pittsburgh (US)
Howard Hughes Medical Institute (US)
Corresponding author: Flavell, Richard A
ORCID: Booth, Carmen J
Nakae, Susumu
Iwakura, Yoichiro
Kolls, Jay K
Flavell, Richard A
Venue: Nature Immunology
Publisher: Springer Science and Business Media LLC
Published: 2009-05-17
Volume: 10
Issue: 6
Pages: 603-609
ISSN: 1529-2908 (ISSN-L)
1529-2916
DOI: 10.1038/ni.1736
PMC: PMC2709990
OpenAlex: W2069571875
Cited by: 756
References: 36
Citations by year: 2026: 7 · 2025: 15 · 2024: 27 · 2023: 26 · 2022: 28 · 2021: 38 · 2020: 32 · 2019: 42 · 2018: 37 · 2017: 36 · 2016: 33 · 2015: 48 · 2014: 61 · 2013: 63 · 2012: 80
FWCI: 37.68
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: Howard Hughes Medical Institute
National Institute on Aging (R00AG029726)
National Heart, Lung, and Blood Institute (R37HL079142)
Topics: Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Health Sciences › Medicine › Gastroenterology › Inflammatory Bowel Disease
Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords: IL-17A, IL-17 receptor, colitis, inflammatory bowel disease, IL-23, Th1 polarization, Th1 cytokines, wasting disease, protective immunity
MeSH terms: T-bet Transcription Factor, Animals, Cell Differentiation, Cells, Cultured, Colitis, Disease Models, Animal, Interferon-gamma, Lymphocyte Activation, Mice, Inbred BALB C, Leukocyte Common Antigens, Mice, Knockout, Th1 Cells, Adoptive Transfer, Wasting Syndrome, Interleukin-17, T-Box Domain Proteins, Gene Expression Profiling, Cell Proliferation, Mice, Receptors, Interleukin-17

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A protective function for interleukin 17A in T cell–mediated intestinal inflammation

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