Interleukin-23 drives innate and T cell–mediated intestinal inflammation
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Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract involving aberrant activation of innate and adaptive immune responses. We have used two complementary models of IBD to examine the roles of interleukin (IL)-12 family cytokines in bacterially induced intestinal inflammation. Our results clearly show that IL-23, but not IL-12, is essential for the induction of chronic intestinal inflammation mediated by innate or adaptive immune mechanisms. Depletion of IL-23 was associated with decreased proinflammatory responses in the intestine but had little impact on systemic T cell inflammatory responses. These results newly identify IL-23 as a driver of innate immune pathology in the intestine and suggest that selective targeting of IL-23 represents an attractive therapeutic approach in human IBD.
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Subsequent studies established an essential role for the IL-23-Th17 axis in disease pathogenesis.
“whereas subsequent studies established an essential role for the IL-23–Th17 axis in disease pathogenesis (15, 72).”
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 [72]
The Abstract reports a crucial role for IL-23 in mouse models of intestinal inflammation. The Discussion, however, says IL-23–driven Th17 responses may be important but are one of several mechanisms contributing to colitis; it does not establish that the combined IL-23–Th17 axis is essential. Page numbers are not available in our copy. (LLM, conf=0.88)
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- [43]Kullberg, M.C., D. Jankovic, C.G. Feng, S. Hue, P.L. Gorelick, B.S. McKenzie, D.J. Cua, F. Powrie, A.W. Cheever, K.J. Maloy, and A. Sher. 2006. IL-23 is a key mediator of Helicobacter hepaticus–induced T cell–dependent colitis. J. Exp. Med. 203: 2485–2494. 17030948 PMC2118119
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- Authors
- Hue, S., Ahern, P., Buonocore, S., Kullberg, M. C., Cua, D. J., McKenzie, B. S., Powrie, F., & Maloy, K. J.
- Affiliations
- 1Sir William Dunn School of Pathology, University of Oxford, Oxford OX1 3RE, England, UK
- University of Oxford (GB)
- University of York (GB)
- 3Department of Discovery Research, Schering-Plough Biopharma, Palo Alto, CA 94304
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2006-10-09
- Volume
- 203
- Issue
- 11
- Pages
- 2473-2483
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2118132
- OpenAlex
- W2133765154
- Cited by
- 823
- References
- 61
- Citations by year
- 2026: 9 · 2025: 15 · 2024: 19 · 2023: 18 · 2022: 18 · 2021: 23 · 2020: 22 · 2019: 45 · 2018: 33 · 2017: 29 · 2016: 36 · 2015: 29 · 2014: 46 · 2013: 50 · 2012: 49
- FWCI
- 47.65
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Minerva Access (University of Melbourne) (submittedVersion, cc-by-nc-sa)
- ENLIGHTEN (Jurnal Bimbingan dan Konseling Islam) (submittedVersion)
- Funders
- Wellcome Trust (070361)
- University of Oxford
- European Commission
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Inflammatory Bowel Disease
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Keywords
- IL-23, IL-12, inflammatory bowel disease, intestinal inflammation, innate immunity, T cell-mediated inflammation
- MeSH terms
- Animals, Immunity, Innate, Mice, Inbred C57BL, T-Lymphocytes, Inflammatory Bowel Diseases, Helicobacter Infections, Mice, Knockout, Helicobacter hepaticus, Mice, Interleukin-23
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