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Complementarity and redundancy of IL-22-producing innate lymphoid cells.
Rankin, Lucille C; Girard-Madoux, Mathilde J H; Seillet, Cyril; Mielke, Lisa A; Kerdiles, Yann; Fenis, Aurore; Wieduwild, Elisabeth; Putoczki, Tracy; Mondot, Stanislas; Lantz, Olivier; Demon, Dieter; Papenfuss, Anthony T; Smyth, Gordon K; Lamkanfi, Mohamed; Carotta, Sebastian; Renauld, Jean-Christophe; Shi, Wei; Carpentier, Sabrina; Soos, Tim; Arendt, Christopher; Ugolini, Sophie; Huntington, Nicholas D; Belz, Gabrielle T; Vivier, Eric.
Afiliação
  • Rankin LC; The Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.
  • Girard-Madoux MJ; Department of Medical Biology, University of Melbourne, Parkville, Australia.
  • Seillet C; Centre d'Immunologie de Marseille-Luminy, Université d'Aix-Marseille UM2, Inserm, U1104, CNRS UMR7280, Marseille, France.
  • Mielke LA; The Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.
  • Kerdiles Y; Department of Medical Biology, University of Melbourne, Parkville, Australia.
  • Fenis A; The Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.
  • Wieduwild E; Department of Medical Biology, University of Melbourne, Parkville, Australia.
  • Putoczki T; Centre d'Immunologie de Marseille-Luminy, Université d'Aix-Marseille UM2, Inserm, U1104, CNRS UMR7280, Marseille, France.
  • Mondot S; Centre d'Immunologie de Marseille-Luminy, Université d'Aix-Marseille UM2, Inserm, U1104, CNRS UMR7280, Marseille, France.
  • Lantz O; Centre d'Immunologie de Marseille-Luminy, Université d'Aix-Marseille UM2, Inserm, U1104, CNRS UMR7280, Marseille, France.
  • Demon D; The Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.
  • Papenfuss AT; Department of Medical Biology, University of Melbourne, Parkville, Australia.
  • Smyth GK; Labex Milieu Intérieur, Institut Pasteur, Paris, France.
  • Lamkanfi M; Laboratoire d'Immunologie and Inserm U932, Institut Curie, Paris, France.
  • Carotta S; Inflammation Research Center, VIB, Ghent University, Ghent, Belgium.
  • Renauld JC; Department of Biochemistry, Ghent University, Ghent, Belgium.
  • Shi W; The Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.
  • Carpentier S; Department of Medical Biology, University of Melbourne, Parkville, Australia.
  • Soos T; The Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.
  • Arendt C; Department of Medical Biology, University of Melbourne, Parkville, Australia.
  • Ugolini S; Department of Mathematics and Statistics, University of Melbourne, Parkville, Australia.
  • Huntington ND; Inflammation Research Center, VIB, Ghent University, Ghent, Belgium.
  • Belz GT; Department of Biochemistry, Ghent University, Ghent, Belgium.
  • Vivier E; The Walter and Eliza Hall Institute of Medical Research, and Department of Medical Biology, University of Melbourne, Parkville, Australia.
Nat Immunol ; 17(2): 179-86, 2016 Feb.
Article em En | MEDLINE | ID: mdl-26595889
ABSTRACT
Intestinal T cells and group 3 innate lymphoid cells (ILC3 cells) control the composition of the microbiota and gut immune responses. Within the gut, ILC3 subsets coexist that either express or lack the natural cytoxicity receptor (NCR) NKp46. We identified here the transcriptional signature associated with the transcription factor T-bet-dependent differentiation of NCR(-) ILC3 cells into NCR(+) ILC3 cells. Contrary to the prevailing view, we found by conditional deletion of the key ILC3 genes Stat3, Il22, Tbx21 and Mcl1 that NCR(+) ILC3 cells were redundant for the control of mouse colonic infection with Citrobacter rodentium in the presence of T cells. However, NCR(+) ILC3 cells were essential for cecal homeostasis. Our data show that interplay between intestinal ILC3 cells and adaptive lymphocytes results in robust complementary failsafe mechanisms that ensure gut homeostasis.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Contexto em Saúde: 3_ND / 6_ODS3_enfermedades_notrasmisibles Problema de saúde: 3_neglected_diseases / 3_zoonosis / 6_malnutrition_nutritional_deficiencies Assunto principal: Linfócitos / Interleucinas / Imunidade Inata Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Nat Immunol Assunto da revista: ALERGIA E IMUNOLOGIA Ano de publicação: 2016 Tipo de documento: Article País de afiliação: Austrália
Texto completo
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Contexto em Saúde: 3_ND / 6_ODS3_enfermedades_notrasmisibles Problema de saúde: 3_neglected_diseases / 3_zoonosis / 6_malnutrition_nutritional_deficiencies Assunto principal: Linfócitos / Interleucinas / Imunidade Inata Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Nat Immunol Assunto da revista: ALERGIA E IMUNOLOGIA Ano de publicação: 2016 Tipo de documento: Article País de afiliação: Austrália