دورية أكاديمية
ILC2s mediate systemic innate protection by priming mucus production at distal mucosal sites.
| العنوان: | ILC2s mediate systemic innate protection by priming mucus production at distal mucosal sites. |
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| المؤلفون: | Campbell L; Wellcome Trust Centre for Cell Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.; Lydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK., Hepworth MR; Lydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.; Manchester Centre for Collaborative Inflammation Research, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK., Whittingham-Dowd J; Wellcome Trust Centre for Cell Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.; Lydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK., Thompson S; Wellcome Trust Centre for Cell Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.; Lydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK., Bancroft AJ; Wellcome Trust Centre for Cell Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.; Lydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK., Hayes KS; Wellcome Trust Centre for Cell Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.; Lydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK., Shaw TN; Lydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.; Manchester Centre for Collaborative Inflammation Research, School of Biological Sciences, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK., Dickey BF; Department of Pulmonary Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX., Flamar AL; Jill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY., Artis D; Jill Roberts Institute for Research in Inflammatory Bowel Disease, Joan and Sanford I. Weill Department of Medicine, Department of Microbiology and Immunology, Weill Cornell Medicine, Cornell University, New York, NY., Schwartz DA; University of Colorado, School of Medicine, Department of Medicine, Aurora, CO., Evans CM; University of Colorado Denver School of Medicine, Division of Pulmonary Sciences and Critical Care Medicine, Aurora, CO., Roberts IS; Lydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK i.s.roberts@manchester.ac.uk., Thornton DJ; Wellcome Trust Centre for Cell Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK Dave.Thornton@manchester.ac.uk.; Lydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK., Grencis RK; Wellcome Trust Centre for Cell Matrix Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK Richard.Grencis@manchester.ac.uk.; Lydia Becker Institute of Immunology and Inflammation, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK. |
| المصدر: | The Journal of experimental medicine [J Exp Med] 2019 Dec 02; Vol. 216 (12), pp. 2714-2723. Date of Electronic Publication: 2019 Oct 03. |
| نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Rockefeller University Press Country of Publication: United States NLM ID: 2985109R Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1540-9538 (Electronic) Linking ISSN: 00221007 NLM ISO Abbreviation: J Exp Med Subsets: MEDLINE |
| أسماء مطبوعة: | Original Publication: New York, NY : Rockefeller University Press |
| مواضيع طبية MeSH: | Immunity, Innate*, Lymphocyte Subsets/*immunology , Lymphocyte Subsets/*metabolism , Mucous Membrane/*immunology , Mucous Membrane/*metabolism , Mucus/*metabolism, Animals ; Cross Protection/immunology ; Goblet Cells/cytology ; Goblet Cells/metabolism ; Hyperplasia ; Interleukin-13/metabolism ; Intestinal Mucosa/immunology ; Intestinal Mucosa/metabolism ; Intestinal Mucosa/parasitology ; Male ; Mice ; Mice, Knockout ; Mucins/biosynthesis ; Trichinella spiralis/immunology ; Trichinellosis/immunology ; Trichinellosis/parasitology |
| مستخلص: | Host immunity to parasitic nematodes requires the generation of a robust type 2 cytokine response, characterized by the production of interleukin 13 (IL-13), which drives expulsion. Here, we show that infection with helminths in the intestine also induces an ILC2-driven, IL-13-dependent goblet cell hyperplasia and increased production of mucins (Muc5b and Muc5ac) at distal sites, including the lungs and other mucosal barrier sites. Critically, we show that type 2 priming of lung tissue through increased mucin production inhibits the progression of a subsequent lung migratory helminth infection and limits its transit through the airways. These data show that infection by gastrointestinal-dwelling helminths induces a systemic innate mucin response that primes peripheral barrier sites for protection against subsequent secondary helminth infections. These data suggest that innate-driven priming of mucus barriers may have evolved to protect from subsequent infections with multiple helminth species, which occur naturally in endemic areas. (© 2019 Campbell et al.) |
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| معلومات مُعتمدة: | R35 HL140039 United States HL NHLBI NIH HHS; T32 HL007085 United States HL NHLBI NIH HHS; R01 HL097163 United States HL NHLBI NIH HHS; United Kingdom WT_ Wellcome Trust; R33 HL120770 United States HL NHLBI NIH HHS; R01 HL129795 United States HL NHLBI NIH HHS; R01 HL130938 United States HL NHLBI NIH HHS; 105610 United Kingdom WT_ Wellcome Trust; R01 HL080396 United States HL NHLBI NIH HHS |
| المشرفين على المادة: | 0 (Interleukin-13) 0 (Mucins) |
| تواريخ الأحداث: | Date Created: 20191005 Date Completed: 20200615 Latest Revision: 20230115 |
| رمز التحديث: | 20240628 |
| مُعرف محوري في PubMed: | PMC6888984 |
| DOI: | 10.1084/jem.20180610 |
| PMID: | 31582416 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 1540-9538 |
|---|---|
| DOI: | 10.1084/jem.20180610 |