{"doi":"10.1084/jem.20101712","title":"IL-23–responsive innate lymphoid cells are increased in inflammatory bowel disease","abstract":"<jats:p>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.</jats:p>","journal":"Journal of Experimental Medicine","year":2011,"id":589598,"datarank":11.267167089737208,"base_score":6.447305862541213,"endowment":6.447305862541213,"self_citation_contribution":0.967095879381182,"citation_network_contribution":10.300071210356027,"self_endowment_contribution":0.967095879381182,"citer_contribution":10.300071210356027,"corpus_percentile":null,"corpus_rank":null,"citation_count":630,"citer_count":200,"citers_with_citation_signal":200,"citers_with_endowment":200,"datacite_reuse_total":6,"is_dataset":false,"is_dataset_confidence":null,"is_data_producer":false,"deposit_databanks":null,"is_oa":false,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":null,"fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":555605,"name":"Carolina V. 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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.</jats:p>","is_dataset_classified":null,"base_score":6.447305862541213,"endowment":6.447305862541213,"datacite_reuse_total":6,"file_count":0,"downloads":0,"views":0,"has_version_chain":false,"is_dataset":false,"is_oa":false,"pmid":"21576383","pmcid":null,"openalex_id":"https://openalex.org/W2166761831","authors":[],"funders":[{"funder_name":"Wellcome Trust","grant_id":"unidentified","title":"unidentified"}],"total_grants":1,"fwci":16.9951,"citation_percentile":0.99623223,"influential_citations":0,"citation_trend":[{"year":2012,"count":32},{"year":2013,"count":49},{"year":2014,"count":55},{"year":2015,"count":45},{"year":2016,"count":53},{"year":2017,"count":66},{"year":2018,"count":54},{"year":2019,"count":54},{"year":2020,"count":43},{"year":2021,"count":46},{"year":2022,"count":45},{"year":2023,"count":24},{"year":2024,"count":21},{"year":2025,"count":25},{"year":2026,"count":5}],"oa_status":"bronze","license":"CC BY NC SA","oa_locations":[{"url":"https://rupress.org/jem/article-pdf/208/6/1127/1205034/jem_20101712.pdf","host_type":"journal"},{"url":"https://rupress.org/jem/article-pdf/208/6/1127/1205034/jem_20101712.pdf","host_type":"publisher"},{"url":"https://rupress.org/jem/article-pdf/208/6/1127/1903700/jem_20101712.pdf","host_type":"publisher"},{"url":"https://doi.org/10.1084/jem.20101712","host_type":"journal"},{"url":"https://pubmed.ncbi.nlm.nih.gov/21576383","host_type":"repository"},{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/3173242","host_type":"repository"},{"url":"https://ora.ox.ac.uk/objects/uuid:19ad829e-9a83-4419-99f5-e00bfffb5f17","host_type":"repository"},{"url":"http://jem.rupress.org/content/208/6/1127.full.pdf","host_type":""},{"url":"http://dx.doi.org/10.1084/jem.20101712","host_type":""},{"url":"https://dx.doi.org/10.1084/jem.20101712","host_type":""}],"fields_of_study":["IL-33, ST2, and ILC Pathways","Whipple's Disease and Interleukins","Immune Cell Function and Interaction","0301 basic medicine","03 medical and health sciences","0302 clinical medicine"],"mesh_terms":["Animals","Biopsy","Cell Separation","Colitis, Ulcerative","Crohn Disease","Gene Expression Regulation","Humans","Leukocytes, Mononuclear","Lymphocytes","Inflammatory Bowel Diseases","Cytokines","CD3 Complex","CD56 Antigen","Interleukin-17","Mice","Interleukin-7 Receptor alpha Subunit","Interleukin-23"],"keywords":["Innate lymphoid cell","Immunology","Interleukin 22","Inflammation","Inflammatory bowel disease","Interleukin 23","Population","Interleukin-7 receptor","Biology","Cytokine","Ulcerative colitis","Pathogenesis","Interleukin 17","Innate immune system","Disease","Interleukin","Medicine","T cell","Pathology","Immune system","IL-2 receptor","CD3 Complex","Biopsy","Interleukin-17","Brief Definitive Report","Cell Separation","Inflammatory Bowel Diseases","Interleukin-23","CD56 Antigen","Interleukin-7 Receptor alpha Subunit","Mice","Crohn Disease","Gene Expression Regulation","Leukocytes, Mononuclear","Animals","Cytokines","Humans","Colitis, Ulcerative","Lymphocytes"],"sdg_mappings":[{"sdg_number":3,"sdg_label":"3. 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