IL-22 is produced by γC-independent CD25+ CCR6+ innate murine spleen cells upon inflammatory stimuli and contributes to LPS-induced lethality.

Laure Dumoutier 1, 2 Magali De Heusch 1, 2 Ciriana Orabona 1, 2 Naoko Satoh-Takayama 3 Gerard Eberl 4 Jean-Claude Sirard 5 James Di Santo 3 Jean-Christophe Renauld 1, 2
1 Ludwig Institute for Cancer Research
2 Experimental Medicine Unit
3 Immunité Innée
4 Développement des Tissus Lymphoïdes
5 CIIL - Centre d’Infection et d’Immunité de Lille (CIIL) - U1019 - UMR 8204
Abstract : IL-22 is a Th17 cytokine that plays a key role in immune responses against extracellular bacteria. In mucosal lymphoid tissues, IL-22 production is mainly due to an IL-23-responsive NK-like cell subset that shares some markers with lymphoid tissue inducer (LTi) cells. Here, we identified a new spleen cell population responsible for IL-22 production upon either in vitro stimulation by anti-CD3 antibodies or in vivo stimulation by lipopolysaccharide (LPS) via IL-2- and an IL-23-dependent mechanisms, respectively. These cells represent 1% of spleen cells from recombination activating gene (Rag2)-deficient mice, and correspond to a discrete innate lymphoid cell population expressing CD25, CCR6 and IL-7R. This population comprises 60-70% CD4(+) cells, which produce IL-22, and are still present in common γ chain-deficient mice; the CD4(-) subset coexpresses IL-22 and IL-17, and is common γ chain-dependent. The importance of IL-22 production for the LPS-triggered response is highlighted by the fact that IL-22-deficient mice are more resistant to LPS-induced mortality.
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European Journal of Immunology, Wiley-VCH Verlag, 2011, 41 (4), pp.1075-85. 〈10.1002/eji.201040878〉
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http://www.hal.inserm.fr/inserm-00926611
Contributeur : Jean-Claude Sirard <>
Soumis le : jeudi 9 janvier 2014 - 21:41:19
Dernière modification le : lundi 8 octobre 2018 - 17:44:07

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Laure Dumoutier, Magali De Heusch, Ciriana Orabona, Naoko Satoh-Takayama, Gerard Eberl, et al.. IL-22 is produced by γC-independent CD25+ CCR6+ innate murine spleen cells upon inflammatory stimuli and contributes to LPS-induced lethality.. European Journal of Immunology, Wiley-VCH Verlag, 2011, 41 (4), pp.1075-85. 〈10.1002/eji.201040878〉. 〈inserm-00926611〉

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