دورية أكاديمية
Group 3 innate lymphoid cells mediate early protective immunity against tuberculosis.
| العنوان: | Group 3 innate lymphoid cells mediate early protective immunity against tuberculosis. |
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| المؤلفون: | Ardain A; Africa Health Research Institute, Durban, South Africa.; School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, South Africa., Domingo-Gonzalez R; Department of Molecular Microbiology, Washington University School of Medicine, St Louis, MO, USA., Das S; Department of Molecular Microbiology, Washington University School of Medicine, St Louis, MO, USA., Kazer SW; Institute for Medical Engineering and Science, Department of Chemistry, Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA.; Ragon Institute of MGH, MIT and Harvard, Cambridge, MA, USA.; Broad Institute of MIT and Harvard, Cambridge, MA, USA., Howard NC; Department of Molecular Microbiology, Washington University School of Medicine, St Louis, MO, USA., Singh A; Africa Health Research Institute, Durban, South Africa.; School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, South Africa., Ahmed M; Department of Molecular Microbiology, Washington University School of Medicine, St Louis, MO, USA., Nhamoyebonde S; Africa Health Research Institute, Durban, South Africa.; School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, South Africa., Rangel-Moreno J; Division of Allergy, Immmunology and Rheumatology, Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA., Ogongo P; Africa Health Research Institute, Durban, South Africa.; School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, South Africa.; Department of Tropical and Infectious Diseases, Institute of Primate Research, Nairobi, Kenya., Lu L; Department of Molecular Microbiology, Washington University School of Medicine, St Louis, MO, USA., Ramsuran D; School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, South Africa., de la Luz Garcia-Hernandez M; Division of Allergy, Immmunology and Rheumatology, Department of Medicine, University of Rochester Medical Center, Rochester, NY, USA., K Ulland T; Division of Immunobiology, Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO, USA., Darby M; IDM, University of Cape Town, Cape Town, South Africa., Park E; Division of Immunobiology, Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO, USA.; Howard Hughes Medical Institute, Washington University School of Medicine, St Louis, MO, USA., Karim F; Africa Health Research Institute, Durban, South Africa., Melocchi L; Division of Immunobiology, Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO, USA., Madansein R; Department of Cardiothoracic Surgery, Nelson Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa., Dullabh KJ; Department of Cardiothoracic Surgery, Nelson Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa., Dunlap M; Department of Molecular Microbiology, Washington University School of Medicine, St Louis, MO, USA., Marin-Agudelo N; Department of Molecular Microbiology, Washington University School of Medicine, St Louis, MO, USA., Ebihara T; Division of Immunobiology, Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO, USA.; Howard Hughes Medical Institute, Washington University School of Medicine, St Louis, MO, USA., Ndung'u T; Africa Health Research Institute, Durban, South Africa.; School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, South Africa., Kaushal D; Tulane National Primate Research Center, Covington, LA, USA., Pym AS; Africa Health Research Institute, Durban, South Africa.; School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, South Africa., Kolls JK; Tulane University Health Sciences, New Orleans, LA, USA., Steyn A; Africa Health Research Institute, Durban, South Africa.; School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, South Africa.; Department of Microbiology, Centres for AIDS Research and Free Radical Biology, University of Alabama at Birmingham, Birmingham, AL, USA., Zúñiga J; Instituto Nacional de Enfermedades Respiratorias Ismael Cosio Villegas, Mexico City, Mexico.; Tecnologico de Monterrey, Escuela de Medicina y Ciencias de la Salud, Mexico City, Mexico., Horsnell W; IDM, University of Cape Town, Cape Town, South Africa.; Institute of Microbiology and Infection, College of Medical and Dental Sciences, University of Birmingham, Birmingham, UK., Yokoyama WM; Division of Immunobiology, Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO, USA.; Howard Hughes Medical Institute, Washington University School of Medicine, St Louis, MO, USA.; Division of Rheumatology, Department of Medicine, Washington University School of Medicine, St Louis, MO, USA., Shalek AK; Institute for Medical Engineering and Science, Department of Chemistry, Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA, USA.; Ragon Institute of MGH, MIT and Harvard, Cambridge, MA, USA.; Broad Institute of MIT and Harvard, Cambridge, MA, USA., Kløverpris HN; Africa Health Research Institute, Durban, South Africa.; School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, South Africa.; Department of Immunology and Microbiology, University of Copenhagen, Copenhagen, Denmark.; Department of Infection and Immunity, University College London, London, UK., Colonna M; Division of Immunobiology, Department of Pathology and Immunology, Washington University School of Medicine, St Louis, MO, USA., Leslie A; Africa Health Research Institute, Durban, South Africa. al.leslie@ahri.org.; School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, Durban, South Africa. al.leslie@ahri.org.; Department of Infection and Immunity, University College London, London, UK. al.leslie@ahri.org., Khader SA; Department of Molecular Microbiology, Washington University School of Medicine, St Louis, MO, USA. sakhader@wustl.edu. |
| المصدر: | Nature [Nature] 2019 Jun; Vol. 570 (7762), pp. 528-532. Date of Electronic Publication: 2019 Jun 05. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. |
| اللغة: | English |
| بيانات الدورية: | Publisher: Nature Publishing Group Country of Publication: England NLM ID: 0410462 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-4687 (Electronic) Linking ISSN: 00280836 NLM ISO Abbreviation: Nature Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Basingstoke : Nature Publishing Group Original Publication: London, Macmillan Journals ltd. |
| مواضيع طبية MeSH: | Immunity, Innate/*immunology , Lymphocytes/*classification , Lymphocytes/*immunology , Macrophages, Alveolar/*immunology , Mycobacterium tuberculosis/*immunology , Tuberculosis, Pulmonary/*immunology , Tuberculosis, Pulmonary/*microbiology, Animals ; Chemokine CXCL13/immunology ; Female ; Granuloma/immunology ; Granuloma/pathology ; Humans ; Interleukin-17/immunology ; Interleukins/immunology ; Lung/immunology ; Lung/microbiology ; Lung/pathology ; Lymphocytes/metabolism ; Macrophages, Alveolar/metabolism ; Male ; Mice ; Receptors, CXCR5/immunology ; Transcriptome/genetics ; Tuberculosis, Pulmonary/genetics ; Interleukin-22 |
| مستخلص: | Tuberculosis is the leading cause of death by an infectious disease worldwide 1 . However, the involvement of innate lymphoid cells (ILCs) in immune responses to infection with Mycobacterium tuberculosis (Mtb) is unknown. Here we show that circulating subsets of ILCs are depleted from the blood of participants with pulmonary tuberculosis and restored upon treatment. Tuberculosis increased accumulation of ILC subsets in the human lung, coinciding with a robust transcriptional response to infection, including a role in orchestrating the recruitment of immune subsets. Using mouse models, we show that group 3 ILCs (ILC3s) accumulated rapidly in Mtb-infected lungs and coincided with the accumulation of alveolar macrophages. Notably, mice that lacked ILC3s exhibited a reduction in the accumulation of early alveolar macrophages and decreased Mtb control. We show that the C-X-C motif chemokine receptor 5 (CXCR5)-C-X-C motif chemokine ligand 13 (CXCL13) axis is involved in Mtb control, as infection upregulates CXCR5 on circulating ILC3s and increases plasma levels of its ligand, CXCL13, in humans. Moreover, interleukin-23-dependent expansion of ILC3s in mice and production of interleukin-17 and interleukin-22 were found to be critical inducers of lung CXCL13, early innate immunity and the formation of protective lymphoid follicles within granulomas. Thus, we demonstrate an early protective role for ILC3s in immunity to Mtb infection. |
| التعليقات: | Erratum in: Nature. 2019 Jul 24;:. (PMID: 31337923) Comment in: Front Immunol. 2020 Aug 27;11:1925. (PMID: 32973795) |
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| معلومات مُعتمدة: | R01 AI134236 United States AI NIAID NIH HHS; 210662/Z/18/Z United Kingdom WT_ Wellcome Trust; R01 AI111914 United States AI NIAID NIH HHS; T32 HL007317 United States HL NHLBI NIH HHS; R01 HL105427 United States HL NHLBI NIH HHS; T32 AI007163 United States AI NIAID NIH HHS; T32 AI007172 United States AI NIAID NIH HHS; U24 AI118672 United States AI NIAID NIH HHS; U19 AI091036 United States AI NIAID NIH HHS; R35 HL139930 United States HL NHLBI NIH HHS; R01 AI123780 United States AI NIAID NIH HHS |
| المشرفين على المادة: | 0 (CXCL13 protein, human) 0 (CXCR5 protein, human) 0 (Chemokine CXCL13) 0 (Cxcl13 protein, mouse) 0 (Interleukin-17) 0 (Interleukins) 0 (Receptors, CXCR5) |
| تواريخ الأحداث: | Date Created: 20190607 Date Completed: 20200304 Latest Revision: 20231213 |
| رمز التحديث: | 20231215 |
| مُعرف محوري في PubMed: | PMC6626542 |
| DOI: | 10.1038/s41586-019-1276-2 |
| PMID: | 31168092 |
| قاعدة البيانات: | MEDLINE |
Find this article in full text from Springer Verlag. 
Full Text Finder | تدمد: | 1476-4687 |
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| DOI: | 10.1038/s41586-019-1276-2 |