Interleukin-23 and Th17 Cells in the Control of Gut Inflammation
Crohn's Disease and Ulcerative Colitis, the major forms of inflammatory bowel diseases (IBDs) in humans, have been traditionally associated with exaggerated and poorly controlled T helper (Th) type 1 or Th2 cell response, respectively. More recent studies have, however, shown that IBDs are als...
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| Format: | Article |
| Language: | English |
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Wiley
2009-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2009/297645 |
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| _version_ | 1832550256323067904 |
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| author | Ivan Monteleone Francesco Pallone Giovanni Monteleone |
| author_facet | Ivan Monteleone Francesco Pallone Giovanni Monteleone |
| author_sort | Ivan Monteleone |
| collection | DOAJ |
| description | Crohn's Disease and Ulcerative Colitis, the major forms of inflammatory bowel diseases (IBDs) in humans, have been traditionally associated with exaggerated and poorly controlled T helper (Th) type 1 or Th2 cell response, respectively. More recent studies have, however, shown that IBDs are also characterized by a sustained production of cytokines made by a distinct lineage of Th cells, termed Th17 cells. The demonstration that Th17-related cytokines cause pathology in many organs, including the gut, and that expansion and maintenance of Th17 cell responses require the activity of IL-23, a cytokine made in excess in the gut of IBD patients has contributed to elucidate new pathways of intestinal tissue damage as well as to design new therapeutic strategies. In this review, we discuss the available data supporting the role of the IL-23/Th17 axis in the modulation of intestinal tissue inflammation. |
| format | Article |
| id | doaj-art-145e471f9e9c4ae88dcb83366ecf10a8 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2009-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-145e471f9e9c4ae88dcb83366ecf10a82025-02-03T06:07:10ZengWileyMediators of Inflammation0962-93511466-18612009-01-01200910.1155/2009/297645297645Interleukin-23 and Th17 Cells in the Control of Gut InflammationIvan Monteleone0Francesco Pallone1Giovanni Monteleone2Department of Internal Medicine, University “Tor Vergata” of Rome, 00133 Rome, ItalyDepartment of Internal Medicine, University “Tor Vergata” of Rome, 00133 Rome, ItalyDepartment of Internal Medicine, University “Tor Vergata” of Rome, 00133 Rome, ItalyCrohn's Disease and Ulcerative Colitis, the major forms of inflammatory bowel diseases (IBDs) in humans, have been traditionally associated with exaggerated and poorly controlled T helper (Th) type 1 or Th2 cell response, respectively. More recent studies have, however, shown that IBDs are also characterized by a sustained production of cytokines made by a distinct lineage of Th cells, termed Th17 cells. The demonstration that Th17-related cytokines cause pathology in many organs, including the gut, and that expansion and maintenance of Th17 cell responses require the activity of IL-23, a cytokine made in excess in the gut of IBD patients has contributed to elucidate new pathways of intestinal tissue damage as well as to design new therapeutic strategies. In this review, we discuss the available data supporting the role of the IL-23/Th17 axis in the modulation of intestinal tissue inflammation.http://dx.doi.org/10.1155/2009/297645 |
| spellingShingle | Ivan Monteleone Francesco Pallone Giovanni Monteleone Interleukin-23 and Th17 Cells in the Control of Gut Inflammation Mediators of Inflammation |
| title | Interleukin-23 and Th17 Cells in the Control of Gut Inflammation |
| title_full | Interleukin-23 and Th17 Cells in the Control of Gut Inflammation |
| title_fullStr | Interleukin-23 and Th17 Cells in the Control of Gut Inflammation |
| title_full_unstemmed | Interleukin-23 and Th17 Cells in the Control of Gut Inflammation |
| title_short | Interleukin-23 and Th17 Cells in the Control of Gut Inflammation |
| title_sort | interleukin 23 and th17 cells in the control of gut inflammation |
| url | http://dx.doi.org/10.1155/2009/297645 |
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