The DOI matches its Crossref record; 10 of the 10 references it cites were found in a registry or an index.
The Proinflammatory Effect of Prostaglandin E2 in Experimental Inflammatory Bowel Disease Is Mediated through the IL-23→IL-17 Axis
Abstract
Although Crohn’s disease has been traditionally considered to be Th1-mediated, the newly identified Th17 cells emerged recently as crucial participants. Th1/Th17 differentiation is controlled primarily by the IL-12 family of cytokines secreted by activated dendritic cells (DCs) and macrophages. IL-23 and IL-12/IL-27 have opposite effects, supporting the Th17 and Th1 phenotypes, respectively. We found that PGE2, a major lipid mediator released in inflammatory conditions, shifts the IL-12/IL-23 balance in DCs in favor of IL-23, and propose that high levels of PGE2 exacerbate the inflammatory process in inflammatory bowel disease through the IL-23→IL-17 axis. We assessed the effects of PGE2 on IL-12, IL-27, and IL-23 and found that PGE2 promotes IL-23, inhibits IL-12 and IL-27 expression and release from stimulated DCs, and subsequently induces IL-17 production in activated T cells. The effects of PGE2 are mediated through the EP2/EP4 receptors on DCs. In vivo, we assessed the effects of PGE analogs in an experimental model for inflammatory bowel disease and found that the exacerbation of clinical symptoms and histopathology correlated with an increase in IL-23 and IL-17, a decrease in IL-12p35 expression in colon and mesenteric lymph nodes, and a substantial increase in the number of infiltrating neutrophils and of CD4+IL-17+ T cells in the colonic tissue. These studies suggest that high levels of PGE2 exacerbate the inflammatory process through the preferential expression and release of DC-derived IL-23 and the subsequent support of the autoreactive/inflammatory Th17 phenotype.
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A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
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IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
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Transforming growth factor-β induces development of the TH17 lineage
Mangan, P. R., Harrington, L. E., O'Quinn, D. B., Helms, W. S., Bullard, D. C., Elson, C. O., Hatton, R. D., Wahl, S. M., Schoeb, T. R., & Weaver, C. T. (2006) · Nature · doi:10.1038/nature04754 · Cited by 3,087
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Divergent Pro- and Antiinflammatory Roles for IL-23 and IL-12 in Joint Autoimmune Inflammation
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IL-17 plays an important role in the development of experimental autoimmune encephalomyelitis
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Interleukin-23 drives innate and T cell–mediated intestinal inflammation
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Wang, D., & DuBois, R. N. (2010) · Oncogene · doi:10.1038/onc.2009.421 · Cited by 805
Yao, C., Sakata, D., Esaki, Y., Li, Y., Matsuoka, T., Kuroiwa, K., Sugimoto, Y., & Narumiya, S. (2009) · Nature Medicine · doi:10.1038/nm.1968 · Cited by 566
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Kumar, V., & Sharma, A. (2010) · International Immunopharmacology · doi:10.1016/j.intimp.2010.08.012 · Cited by 444
Protumor vs Antitumor Functions of IL-17
Murugaiyan, G., & Saha, B. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0901017 · Cited by 369
Metadata
- Authors
- Sheibanie, A. F., Yen, J.-H., Khayrullina, T., Emig, F., Zhang, M., Tuma, R., & Ganea, D.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2007-06
- Volume
- 178
- Issue
- 12
- Pages
- 8138-8147
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W1940681873
- Cited by
- 284
- References
- 10
- FWCI
- 11.39
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: The Proinflammatory Effect of Prostaglandin E2 in Experimental Inflammatory Bowel Disease Is Mediated through the IL-23→IL-17 Axis. https://app.cochat.ai/papers/10.4049/jimmunol.178.12.8138
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- Sheibanie, A. F., Yen, J.-H., Khayrullina, T., Emig, F., Zhang, M., Tuma, R., & Ganea, D. (2007). The Proinflammatory Effect of Prostaglandin E2 in Experimental Inflammatory Bowel Disease Is Mediated through the IL-23→IL-17 Axis. The Journal of Immunology. https://doi.org/10.4049/jimmunol.178.12.8138
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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