Neutrophilic NLRP3 inflammasome-dependent ...
Document type :
Article dans une revue scientifique: Article original
DOI :
PMID :
Title :
Neutrophilic NLRP3 inflammasome-dependent IL-1β secretion regulates the γδT17 cell response in respiratory bacterial infections.
Author(s) :
Hassane, M [Auteur]
Faculté des Sciences
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Demon, D [Auteur]
VIB-UGent Center for Inflammation Research [Gand, Belgique] [IRC]
Universiteit Gent = Ghent University = Université de Gand [UGENT]
Soulard, D [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Fontaine, J [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Keller, Le [Auteur]
Groningen Biomolecular Sciences and Biotechnology Institute [GBB]
Patin, Cédric [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Porte, R [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Prinz, I [Auteur]
Medizinische Hochschule Hannover = Hannover Medical School [MHH]
Ryffel, Bernhard [Auteur]
University of Cape Town
Immunologie et Neurogénétique Expérimentales et Moléculaires [INEM]
Kadioglu, A [Auteur]
Institute of Infection and Global Health [University of Liverpool, UK]
Veening, Jw [Auteur]
Groningen Biomolecular Sciences and Biotechnology Institute [GBB]
Sirard, Jc [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Faveeuw, C [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Lamkanfi, M [Auteur]
VIB-UGent Center for Inflammation Research [Gand, Belgique] [IRC]
Universiteit Gent = Ghent University = Université de Gand [UGENT]
Trottein, F [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Paget, Christophe [Auteur correspondant]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Faculté des Sciences
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Demon, D [Auteur]
VIB-UGent Center for Inflammation Research [Gand, Belgique] [IRC]
Universiteit Gent = Ghent University = Université de Gand [UGENT]
Soulard, D [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Fontaine, J [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Keller, Le [Auteur]
Groningen Biomolecular Sciences and Biotechnology Institute [GBB]
Patin, Cédric [Auteur]

Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Porte, R [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Prinz, I [Auteur]
Medizinische Hochschule Hannover = Hannover Medical School [MHH]
Ryffel, Bernhard [Auteur]
University of Cape Town
Immunologie et Neurogénétique Expérimentales et Moléculaires [INEM]
Kadioglu, A [Auteur]
Institute of Infection and Global Health [University of Liverpool, UK]
Veening, Jw [Auteur]
Groningen Biomolecular Sciences and Biotechnology Institute [GBB]
Sirard, Jc [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Faveeuw, C [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Lamkanfi, M [Auteur]
VIB-UGent Center for Inflammation Research [Gand, Belgique] [IRC]
Universiteit Gent = Ghent University = Université de Gand [UGENT]
Trottein, F [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Paget, Christophe [Auteur correspondant]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Journal title :
Mucosal Immunology
Pages :
1056-1068
Publisher :
Nature Pub. Group
Publication date :
2017-07
ISSN :
1933-0219
HAL domain(s) :
Sciences du Vivant [q-bio]/Microbiologie et Parasitologie
Sciences du Vivant [q-bio]/Immunologie
Sciences du Vivant [q-bio]/Immunologie
English abstract : [en]
Traditionally regarded as simple foot soldiers of the innate immune response limited to the eradication of pathogens, neutrophils recently emerged as more complex cells endowed with a set of immunoregulatory functions. ...
Show more >Traditionally regarded as simple foot soldiers of the innate immune response limited to the eradication of pathogens, neutrophils recently emerged as more complex cells endowed with a set of immunoregulatory functions. Using a model of invasive pneumococcal disease, we highlighted an unexpected key role for neutrophils as accessory cells in innate interleukin (IL)-17A production by lung resident Vγ6Vδ1(+) T cells via nucleotide-binding oligomerization domain receptor, pyrin-containing 3 (NLRP3) inflammasome-dependent IL-1β secretion. In vivo activation of the NLRP3 inflammasome in neutrophils required both host-derived and bacterial-derived signals. Elaborately, it relies on (i) alveolar macrophage-secreted TNF-α for priming and (ii) subsequent exposure to bacterial pneumolysin for activation. Interestingly, this mechanism can be translated to human neutrophils. Our work revealed the cellular and molecular dynamic events leading to γδT17 cell activation, and highlighted for the first time the existence of a fully functional NLRP3 inflammasome in lung neutrophils. This immune axis thus regulates the development of a protective host response to respiratory bacterial infections.Show less >
Show more >Traditionally regarded as simple foot soldiers of the innate immune response limited to the eradication of pathogens, neutrophils recently emerged as more complex cells endowed with a set of immunoregulatory functions. Using a model of invasive pneumococcal disease, we highlighted an unexpected key role for neutrophils as accessory cells in innate interleukin (IL)-17A production by lung resident Vγ6Vδ1(+) T cells via nucleotide-binding oligomerization domain receptor, pyrin-containing 3 (NLRP3) inflammasome-dependent IL-1β secretion. In vivo activation of the NLRP3 inflammasome in neutrophils required both host-derived and bacterial-derived signals. Elaborately, it relies on (i) alveolar macrophage-secreted TNF-α for priming and (ii) subsequent exposure to bacterial pneumolysin for activation. Interestingly, this mechanism can be translated to human neutrophils. Our work revealed the cellular and molecular dynamic events leading to γδT17 cell activation, and highlighted for the first time the existence of a fully functional NLRP3 inflammasome in lung neutrophils. This immune axis thus regulates the development of a protective host response to respiratory bacterial infections.Show less >
Language :
Anglais
Peer reviewed article :
Oui
Audience :
Internationale
Popular science :
Non
Source :
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