The DOI matches its Crossref record; 39 of the 39 references it cites were found in a registry or an index.
IL-23 is essential for T cell–mediated colitis and promotes inflammation via IL-17 and IL-6
Open accessAbstract
Uncontrolled mucosal immunity in the gastrointestinal tract of humans results in chronic inflammatory bowel disease (IBD), such as Crohn disease and ulcerative colitis. In early clinical trials as well as in animal models, IL-12 has been implicated as a major mediator of these diseases based on the ability of anti-p40 mAb treatment to reverse intestinal inflammation. The cytokine IL-23 shares the same p40 subunit with IL-12, and the anti-p40 mAbs used in human and mouse IBD studies neutralized the activities of both IL-12 and IL-23. IL-10-deficient mice spontaneously develop enterocolitis. To determine how IL-23 contributes to intestinal inflammation, we studied the disease susceptibility in the absence of either IL-23 or IL-12 in this model, as well as the ability of recombinant IL-23 to exacerbate IBD induced by T cell transfer. Our study shows that in these models, IL-23 is essential for manifestation of chronic intestinal inflammation, whereas IL-12 is not. A critical target of IL-23 is a unique subset of tissue-homing memory T cells, which are specifically activated by IL-23 to produce the proinflammatory mediators IL-17 and IL-6. This pathway may be responsible for chronic intestinal inflammation as well as other chronic autoimmune inflammatory diseases.
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Citations
Cites
IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
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Self-citationToll Pathway-Dependent Blockade of CD4 + CD25 + T Cell-Mediated Suppression by Dendritic Cells
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Increased expression of interleukin 17 in inflammatory bowel disease
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Divergent Pro- and Antiinflammatory Roles for IL-23 and IL-12 in Joint Autoimmune Inflammation
Murphy, C. A., Langrish, C. L., Chen, Y., Blumenschein, W., McClanahan, T., Kastelein, R. A., Sedgwick, J. D., & Cua, D. J. (2003) · The Journal of Experimental Medicine · doi:10.1084/jem.20030896 · Cited by 1,669
Self-citationAntibodies to interleukin 12 abrogate established experimental colitis in mice.
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Cited by
Ivanov, I. I., McKenzie, B. S., Zhou, L., Tadokoro, C. E., Lepelley, A., Lafaille, J. J., Cua, D. J., & Littman, D. R. (2006) · Cell · doi:10.1016/j.cell.2006.07.035 · Cited by 5,145
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Induction of Intestinal Th17 Cells by Segmented Filamentous Bacteria
Ivanov, I. I., Atarashi, K., Manel, N., Brodie, E. L., Shima, T., Karaoz, U., Wei, D., Goldfarb, K. C., Santee, C. A., Lynch, S. V., et al. (2009) · Cell · doi:10.1016/j.cell.2009.09.033 · Cited by 4,554
Unravelling the pathogenesis of inflammatory bowel disease
Xavier, R. J., & Podolsky, D. K. (2007) · Nature · doi:10.1038/nature06005 · Cited by 4,364
A Genome-Wide Association Study Identifies IL23R as an Inflammatory Bowel Disease Gene
Duerr, R. H., Taylor, K. D., Brant, S. R., Rioux, J. D., Silverberg, M. S., Daly, M. J., Steinhart, A. H., Abraham, C., Regueiro, M., Griffiths, A., et al. (2006) · Science · doi:10.1126/science.1135245 · Cited by 3,039
Metadata
- Authors
- Yen, D., Cheung, J., Scheerens, H., Poulet, F., McClanahan, T., Mckenzie, B., Kleinschek, M. A., Owyang, A., Mattson, J., Blumenschein, W., Murphy, E., Sathe, M., Cua, D. J., Kastelein, R. A., & Rennick, D.
- Venue
- Journal of Clinical Investigation
- Published
- 2006-05-01
- Volume
- 116
- Issue
- 5
- Pages
- 1310-1316
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W2065307318
- Cited by
- 1,542
- References
- 39
- FWCI
- 77.40
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Yen, D., Cheung, J., Scheerens, H., Poulet, F., McClanahan, T., Mckenzie, B., Kleinschek, M. A., Owyang, A., Mattson, J., Blumenschein, W., Murphy, E., Sathe, M., Cua, D. J., Kastelein, R. A., & Rennick, D. (2006). IL-23 is essential for T cell–mediated colitis and promotes inflammation via IL-17 and IL-6. Journal of Clinical Investigation. https://doi.org/10.1172/jci21404
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
