دورية أكاديمية
CD3bright signals on γδ T cells identify IL-17A-producing Vγ6Vδ1+ T cells.
العنوان: | CD3bright signals on γδ T cells identify IL-17A-producing Vγ6Vδ1+ T cells. |
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المؤلفون: | Paget C; 1] Peter MacCallum Cancer Centre, Cancer Immunology Program, St Andrews Place, East Melbourne, Victoria, Australia [2] Sir Peter MacCallum Department of Oncology and Department of Pathology, University of Melbourne, Parkville, Victoria, Australia [3] INSERM U1019, Centre d'Infection et d'Immunité de Lille, Institut Pasteur de Lille, Lille, France [4] University of Lille 2, Lille, France., Chow MT; 1] Peter MacCallum Cancer Centre, Cancer Immunology Program, St Andrews Place, East Melbourne, Victoria, Australia [2] Sir Peter MacCallum Department of Oncology and Department of Pathology, University of Melbourne, Parkville, Victoria, Australia [3] QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia., Gherardin NA; 1] Peter MacCallum Cancer Centre, Cancer Immunology Program, St Andrews Place, East Melbourne, Victoria, Australia [2] Sir Peter MacCallum Department of Oncology and Department of Pathology, University of Melbourne, Parkville, Victoria, Australia [3] Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Parkville, Victoria, Australia., Beavis PA; 1] Peter MacCallum Cancer Centre, Cancer Immunology Program, St Andrews Place, East Melbourne, Victoria, Australia [2] Sir Peter MacCallum Department of Oncology and Department of Pathology, University of Melbourne, Parkville, Victoria, Australia., Uldrich AP; Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Parkville, Victoria, Australia., Duret H; 1] Peter MacCallum Cancer Centre, Cancer Immunology Program, St Andrews Place, East Melbourne, Victoria, Australia [2] Sir Peter MacCallum Department of Oncology and Department of Pathology, University of Melbourne, Parkville, Victoria, Australia., Hassane M; 1] INSERM U1019, Centre d'Infection et d'Immunité de Lille, Institut Pasteur de Lille, Lille, France [2] University of Lille 2, Lille, France., Souza-Fonseca-Guimaraes F; QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia., Mogilenko DA; 1] University of Lille 2, Lille, France [2] INSERM U1011, Institut Pasteur de Lille, Lille, France [3] European Genomic Institute of Diabetes, Lille, France., Staumont-Sallé D; 1] University of Lille 2, Lille, France [2] INSERM U1011, Institut Pasteur de Lille, Lille, France [3] European Genomic Institute of Diabetes, Lille, France [4] Department of Dermatology, Claude Huriez Hospital, Lille, France., Escalante NK; Department of Immunology, University of Toronto, Toronto, Ontario, Canada., Hill GR; 1] QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia [2] Department of Bone Marrow Transplantation, Royal Brisbane Hospital, Herston, Queensland, Australia., Neeson P; 1] Peter MacCallum Cancer Centre, Cancer Immunology Program, St Andrews Place, East Melbourne, Victoria, Australia [2] Sir Peter MacCallum Department of Oncology and Department of Pathology, University of Melbourne, Parkville, Victoria, Australia., Ritchie DS; 1] Peter MacCallum Cancer Centre, Cancer Immunology Program, St Andrews Place, East Melbourne, Victoria, Australia [2] Sir Peter MacCallum Department of Oncology and Department of Pathology, University of Melbourne, Parkville, Victoria, Australia., Dombrowicz D; 1] University of Lille 2, Lille, France [2] INSERM U1011, Institut Pasteur de Lille, Lille, France [3] European Genomic Institute of Diabetes, Lille, France., Mallevaey T; Department of Immunology, University of Toronto, Toronto, Ontario, Canada., Trottein F; 1] INSERM U1019, Centre d'Infection et d'Immunité de Lille, Institut Pasteur de Lille, Lille, France [2] University of Lille 2, Lille, France., Belz GT; Division of Molecular Immunology, Walter and Eliza Hall Institute of Medical Research, Melbourne, Victoria, Australia., Godfrey DI; 1] Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Parkville, Victoria, Australia [2] Australian Research Council Centre of Excellence in Advanced Medical Imaging at University of Melbourne, Parkville, Victoria, Australia., Smyth MJ; 1] Peter MacCallum Cancer Centre, Cancer Immunology Program, St Andrews Place, East Melbourne, Victoria, Australia [2] Sir Peter MacCallum Department of Oncology and Department of Pathology, University of Melbourne, Parkville, Victoria, Australia [3] QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia [4] School of Medicine, University of Queensland, Herston, Queensland, Australia. |
المصدر: | Immunology and cell biology [Immunol Cell Biol] 2015 Feb; Vol. 93 (2), pp. 198-212. Date of Electronic Publication: 2014 Nov 11. |
نوع المنشور: | Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. |
اللغة: | English |
بيانات الدورية: | Publisher: Wiley Country of Publication: United States NLM ID: 8706300 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1440-1711 (Electronic) Linking ISSN: 08189641 NLM ISO Abbreviation: Immunol Cell Biol Subsets: MEDLINE |
أسماء مطبوعة: | Publication: 2018- : [Hoboken, NJ] : Wiley Original Publication: [Adelaide, South Australia] : University of Adelaide, [c1987- |
مواضيع طبية MeSH: | CD3 Complex/*metabolism , Interleukin-17/*biosynthesis , Receptors, Antigen, T-Cell, gamma-delta/*metabolism , T-Lymphocytes/*immunology, Amino Acid Sequence ; Aminoquinolines/pharmacology ; Animals ; CD3 Complex/chemistry ; Carrier Proteins/metabolism ; Germ Cells/drug effects ; Homeostasis/drug effects ; Imiquimod ; Immunity ; Inflammasomes/drug effects ; Inflammasomes/metabolism ; Interleukin-1beta/metabolism ; Interleukin-23 ; Lung/drug effects ; Lung/immunology ; Lymphocyte Subsets/drug effects ; Lymphocyte Subsets/immunology ; Male ; Mice, Inbred C57BL ; Molecular Sequence Data ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; Phenotype ; Skin/drug effects ; Skin/immunology ; T-Lymphocytes/drug effects |
مستخلص: | Interleukin-17A (IL-17A) is a pro-inflammatory cytokine that has an important role at mucosal sites in a wide range of immune responses including infection, allergy and auto-immunity. γδ T cells are recognized as IL-17 producers, but based on the level of CD3 expression, we now define the remarkable ability of a CD3(bright) γδ T-cell subset with an effector memory phenotype to rapidly produce IL-17A, but not interferon-γ. CD3(bright) γδ T cells uniformly express the canonical germline encoded Vγ6/Vδ1(+) T-cell receptor. They are widely distributed with a preferential representation in the lungs and skin are negatively impacted in the absence of retinoic acid receptor-related orphan receptor gammat expression or endogenous flora. This population responded rapidly to various stimuli in a mechanism involving IL-23 and NOD-like receptor family, pyrin domain containing 3 (NLRP3)-inflammasome-dependent IL-1β. Finally, we demonstrated that IL-17-producing CD3(bright) γδ T cells responded promptly and strongly to pneumococcal infection and during skin inflammation. Here, we propose a new way to specifically analyze IL-17-producing Vγ6/Vδ1(+) T cells based on the level of CD3 signals. Using this gating strategy, our data reinforce the crucial role of this γδ T-cell subset in respiratory and skin disorders. |
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المشرفين على المادة: | 0 (Aminoquinolines) 0 (CD3 Complex) 0 (Carrier Proteins) 0 (Inflammasomes) 0 (Interleukin-17) 0 (Interleukin-1beta) 0 (Interleukin-23) 0 (NLR Family, Pyrin Domain-Containing 3 Protein) 0 (Nlrp3 protein, mouse) 0 (Nuclear Receptor Subfamily 1, Group F, Member 3) 0 (Receptors, Antigen, T-Cell, gamma-delta) 0 (T-cell receptor Vgamma6, mouse) P1QW714R7M (Imiquimod) |
تواريخ الأحداث: | Date Created: 20141112 Date Completed: 20151214 Latest Revision: 20220410 |
رمز التحديث: | 20240829 |
DOI: | 10.1038/icb.2014.94 |
PMID: | 25385067 |
قاعدة البيانات: | MEDLINE |
تدمد: | 1440-1711 |
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DOI: | 10.1038/icb.2014.94 |