IL-23-responsive innate lymphoid cells are increased in inflammatory bowel disease.
Results of experimental and genetic studies have highlighted the role of the IL-23/IL-17 axis in the pathogenesis of inflammatory bowel disease (IBD). IL-23-driven inflammation has been primarily linked to Th17 cells; however, we have recently identified a novel population of innate lymphoid cells (...
| Hoofdauteurs: | , , , , , , , |
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| Formaat: | Journal article |
| Taal: | English |
| Gepubliceerd in: |
2011
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| _version_ | 1826261337659932672 |
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| author | Geremia, A Arancibia-Cárcamo, C Fleming, M Rust, N Singh, B Mortensen, N Travis, S Powrie, F |
| author_facet | Geremia, A Arancibia-Cárcamo, C Fleming, M Rust, N Singh, B Mortensen, N Travis, S Powrie, F |
| author_sort | Geremia, A |
| collection | OXFORD |
| description | Results of experimental and genetic studies have highlighted the role of the IL-23/IL-17 axis in the pathogenesis of inflammatory bowel disease (IBD). IL-23-driven inflammation has been primarily linked to Th17 cells; however, we have recently identified a novel population of innate lymphoid cells (ILCs) in mice that produces IL-17, IL-22, and IFN-γ in response to IL-23 and mediates innate colitis. The relevance of ILC populations in human health and disease is currently poorly understood. In this study, we have analyzed the role of IL-23-responsive ILCs in the human intestine in control and IBD patients. Our results show increased expression of the Th17-associated cytokine genes IL17A and IL17F among intestinal CD3⁻ cells in IBD. IL17A and IL17F expression is restricted to CD56⁻ ILCs, whereas IL-23 induces IL22 and IL26 in the CD56⁺ ILC compartment. Furthermore, we observed a significant and selective increase in CD127⁺CD56⁻ ILCs in the inflamed intestine in Crohn's disease (CD) patients but not in ulcerative colitis patients. These results indicate that IL-23-responsive ILCs are present in the human intestine and that intestinal inflammation in CD is associated with the selective accumulation of a phenotypically distinct ILC population characterized by inflammatory cytokine expression. ILCs may contribute to intestinal inflammation through cytokine production, lymphocyte recruitment, and organization of the inflammatory tissue and may represent a novel tissue-specific target for subtypes of IBD. |
| first_indexed | 2024-03-06T19:19:48Z |
| format | Journal article |
| id | oxford-uuid:19ad829e-9a83-4419-99f5-e00bfffb5f17 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T19:19:48Z |
| publishDate | 2011 |
| record_format | dspace |
| spelling | oxford-uuid:19ad829e-9a83-4419-99f5-e00bfffb5f172022-03-26T10:50:19ZIL-23-responsive innate lymphoid cells are increased in inflammatory bowel disease.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:19ad829e-9a83-4419-99f5-e00bfffb5f17EnglishSymplectic Elements at Oxford2011Geremia, AArancibia-Cárcamo, CFleming, MRust, NSingh, BMortensen, NTravis, SPowrie, FResults of experimental and genetic studies have highlighted the role of the IL-23/IL-17 axis in the pathogenesis of inflammatory bowel disease (IBD). IL-23-driven inflammation has been primarily linked to Th17 cells; however, we have recently identified a novel population of innate lymphoid cells (ILCs) in mice that produces IL-17, IL-22, and IFN-γ in response to IL-23 and mediates innate colitis. The relevance of ILC populations in human health and disease is currently poorly understood. In this study, we have analyzed the role of IL-23-responsive ILCs in the human intestine in control and IBD patients. Our results show increased expression of the Th17-associated cytokine genes IL17A and IL17F among intestinal CD3⁻ cells in IBD. IL17A and IL17F expression is restricted to CD56⁻ ILCs, whereas IL-23 induces IL22 and IL26 in the CD56⁺ ILC compartment. Furthermore, we observed a significant and selective increase in CD127⁺CD56⁻ ILCs in the inflamed intestine in Crohn's disease (CD) patients but not in ulcerative colitis patients. These results indicate that IL-23-responsive ILCs are present in the human intestine and that intestinal inflammation in CD is associated with the selective accumulation of a phenotypically distinct ILC population characterized by inflammatory cytokine expression. ILCs may contribute to intestinal inflammation through cytokine production, lymphocyte recruitment, and organization of the inflammatory tissue and may represent a novel tissue-specific target for subtypes of IBD. |
| spellingShingle | Geremia, A Arancibia-Cárcamo, C Fleming, M Rust, N Singh, B Mortensen, N Travis, S Powrie, F IL-23-responsive innate lymphoid cells are increased in inflammatory bowel disease. |
| title | IL-23-responsive innate lymphoid cells are increased in inflammatory bowel disease. |
| title_full | IL-23-responsive innate lymphoid cells are increased in inflammatory bowel disease. |
| title_fullStr | IL-23-responsive innate lymphoid cells are increased in inflammatory bowel disease. |
| title_full_unstemmed | IL-23-responsive innate lymphoid cells are increased in inflammatory bowel disease. |
| title_short | IL-23-responsive innate lymphoid cells are increased in inflammatory bowel disease. |
| title_sort | il 23 responsive innate lymphoid cells are increased in inflammatory bowel disease |
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