Interleukin-22 Is Produced by Invariant ...
Document type :
Compte-rendu et recension critique d'ouvrage
DOI :
PMID :
Title :
Interleukin-22 Is Produced by Invariant Natural Killer T Lymphocytes during Influenza A Virus Infection
Author(s) :
Paget, Christophe [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Ivanov, Stoyan [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Fontaine, Josette [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Renneson, Joelle [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Blanc, Fany [Auteur]
Défense innée et inflammation
Pichavant, Muriel [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Dumoutier, Laure [Auteur]
Université Catholique de Louvain = Catholic University of Louvain [UCL]
Ryffel, Bernhard [Auteur]
Immunologie et Embryologie Moléculaires [IEM]
Renauld, Jean Christophe [Auteur]
Université Catholique de Louvain = Catholic University of Louvain [UCL]
Gosset, Philippe [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Gosset, Pierre [Auteur]
Hôpital Saint Vincent de Paul de Lille
Université catholique de Lille [UCL]
Si-Tahar, Mustapha [Auteur]
Défense innée et inflammation
Faveeuw, Christelle [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Trottein, Francois [Auteur correspondant]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Ivanov, Stoyan [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Fontaine, Josette [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Renneson, Joelle [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Blanc, Fany [Auteur]
Défense innée et inflammation
Pichavant, Muriel [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Dumoutier, Laure [Auteur]
Université Catholique de Louvain = Catholic University of Louvain [UCL]
Ryffel, Bernhard [Auteur]
Immunologie et Embryologie Moléculaires [IEM]
Renauld, Jean Christophe [Auteur]
Université Catholique de Louvain = Catholic University of Louvain [UCL]
Gosset, Philippe [Auteur]
![refId](/themes/Mirage2//images/idref.png)
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Gosset, Pierre [Auteur]
Hôpital Saint Vincent de Paul de Lille
Université catholique de Lille [UCL]
Si-Tahar, Mustapha [Auteur]
Défense innée et inflammation
Faveeuw, Christelle [Auteur]
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Trottein, Francois [Auteur correspondant]
![refId](/themes/Mirage2//images/idref.png)
Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL]
Journal title :
Journal of Biological Chemistry
Pages :
8816-8829
Publisher :
American Society for Biochemistry and Molecular Biology
Publication date :
2012-03-16
ISSN :
0021-9258
English keyword(s) :
Dendritic Cells
Infectious Diseases
Influenza Virus
Innate Immunity
Interleukin
IL-22
Innate Sensors
Natural Killer T Cells
Influenza A Virus
Infectious Diseases
Influenza Virus
Innate Immunity
Interleukin
IL-22
Innate Sensors
Natural Killer T Cells
Influenza A Virus
HAL domain(s) :
Sciences du Vivant [q-bio]/Immunologie
English abstract : [en]
Invariant natural killer T (iNKT) cells are non-conventional lipid-reactive αβ T lymphocytes that play a key role in host responses during viral infections, in particular through the swift production of cytokines. Their ...
Show more >Invariant natural killer T (iNKT) cells are non-conventional lipid-reactive αβ T lymphocytes that play a key role in host responses during viral infections, in particular through the swift production of cytokines. Their beneficial role during experimental influenza A virus (IAV) infection has recently been proposed, although the mechanisms involved remain elusive. Here we show that during in vivo IAV infection, mouse pulmonary iNKT cells produce IFN-γ and IL-22, a Th17-related cytokine critical in mucosal immunity. Although permissive to viral replication, IL-22 production by iNKT cells is not due to IAV infection per se of these cells but is indirectly mediated by IAV-infected dendritic cells (DCs). We show that activation of the viral RNA sensors TLR7 and RIG-I in DCs is important for triggering IL-22 secretion by iNKT cells, whereas the NOD-like receptors NOD2 and NLRP3 are dispensable. Invariant NKT cells respond to IL-1β and IL-23 provided by infected DCs independently of the CD1d molecule to release IL-22. In vitro, IL-22 protects IAV-infected airway epithelial cells against mortality but has no role on viral replication. Finally, during early IAV infection, IL-22 plays a positive role in the control of lung epithelial damages. Overall, IAV infection of DCs activates iNKT cells, providing a rapid source of IL-22 that might be beneficial to preserve the lung epithelium integrity.Show less >
Show more >Invariant natural killer T (iNKT) cells are non-conventional lipid-reactive αβ T lymphocytes that play a key role in host responses during viral infections, in particular through the swift production of cytokines. Their beneficial role during experimental influenza A virus (IAV) infection has recently been proposed, although the mechanisms involved remain elusive. Here we show that during in vivo IAV infection, mouse pulmonary iNKT cells produce IFN-γ and IL-22, a Th17-related cytokine critical in mucosal immunity. Although permissive to viral replication, IL-22 production by iNKT cells is not due to IAV infection per se of these cells but is indirectly mediated by IAV-infected dendritic cells (DCs). We show that activation of the viral RNA sensors TLR7 and RIG-I in DCs is important for triggering IL-22 secretion by iNKT cells, whereas the NOD-like receptors NOD2 and NLRP3 are dispensable. Invariant NKT cells respond to IL-1β and IL-23 provided by infected DCs independently of the CD1d molecule to release IL-22. In vitro, IL-22 protects IAV-infected airway epithelial cells against mortality but has no role on viral replication. Finally, during early IAV infection, IL-22 plays a positive role in the control of lung epithelial damages. Overall, IAV infection of DCs activates iNKT cells, providing a rapid source of IL-22 that might be beneficial to preserve the lung epithelium integrity.Show less >
Language :
Anglais
Popular science :
Non
Source :
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