A protective function for interleukin 17A in T cell–mediated intestinal inflammation
Open accessAbstract
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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IL-17A- and IL-22-producing Th17 cells appear to be protective rather than pathogenic in the intestines.
“Given that IL-17A- and IL-22-producing Th17 cells appear to be protective rather than pathogenic in the intestines (84)”
From T <sub>H</sub> 17 cells require ongoing classic IL-6 receptor signaling to retain transcriptional and functional identity (2020) · cites this paper as [84]
The Results ('IL-17A modulates T cell–driven colitis'; page unavailable) show that IL-17A delayed disease onset in a mouse T-cell-transfer model, supporting a protective role in that setting. The paper does not establish that IL-22-producing Th17 cells are protective; the Discussion reports that IL-22 was not responsible for the accelerated disease seen without IL-17A. The claim also extends a model-specific finding to the intestines generally. (LLM, conf=0.88)
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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
- Venue
- Nature Immunology
- Published
- 2009-05-17
- Volume
- 10
- Issue
- 6
- Pages
- 603-609
- ISSN
- 1529-2908 (ISSN-L)
- 1529-2916
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › 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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