title: AhR modulates the IL-22-producing cell proliferation/recruitment in imiquimod-induced psoriasis mouse model.
abstract: IL-22 has a detrimental role in skin inflammatory processes, for example in psoriasis. As transcription factor, AhR controls the IL-22 production by several cell types (i.e. Th17 cells). Here, we analyzed the role of Ahr in IL-22 production by immune cells in the inflamed skin, using an imiquimod-induced psoriasis mouse model. Our results indicate that IL-22 is expressed in the ear of imiquimod-treated Ahr(-/-) mice but less than in wild-type mice. We then studied the role of AhR on three cell populations known to produce IL-22 in the skin: γδ T cells, Th17 cells, and ILC3, and a novel IL-22-producing cell type identified in this setting: CD4(-) CD8(-) TCRβ(+) T cells. We showed that AhR is required for IL-22 production by Th17, but not by the three other cell types, in the imiquimod-treated ears. Moreover, AhR has a role in the recruitment of γδ T cells, ILC3, and CD4(-) CD8(-) TCRβ(+) T cells into the inflamed skin or in their local proliferation. Taken together, AhR has a direct role in IL-22 production by Th17 cells in the mouse ear skin, but not by γδ T cells, CD4(-) CD8(-) TCRβ(+) T cells and ILCs.
authors.affiliation: Ludwig Institute for Cancer Research, Brussels Branch, Belgium.|de Duve Institute, Université catholique de Louvain, Brussels, Belgium.
authors.forename: Perrine M
authors.initials: PM
authors.lastname: Cochez
authors.affiliation: Ludwig Institute for Cancer Research, Brussels Branch, Belgium.|de Duve Institute, Université catholique de Louvain, Brussels, Belgium.
authors.forename: Camille
authors.initials: C
authors.lastname: Michiels
authors.affiliation: Ludwig Institute for Cancer Research, Brussels Branch, Belgium.|de Duve Institute, Université catholique de Louvain, Brussels, Belgium.
authors.forename: Emilie
authors.initials: E
authors.lastname: Hendrickx
authors.affiliation: Ludwig Institute for Cancer Research, Brussels Branch, Belgium.|de Duve Institute, Université catholique de Louvain, Brussels, Belgium.
authors.forename: Astrid B
authors.initials: AB
authors.lastname: Van Belle
authors.affiliation: Ludwig Institute for Cancer Research, Brussels Branch, Belgium.|de Duve Institute, Université catholique de Louvain, Brussels, Belgium.
authors.forename: Muriel M
authors.initials: MM
authors.lastname: Lemaire
authors.affiliation: de Duve Institute, Université catholique de Louvain, Brussels, Belgium.
authors.forename: Nicolas
authors.initials: N
authors.lastname: Dauguet
authors.affiliation: Ludwig Institute for Cancer Research, Brussels Branch, Belgium.
authors.forename: Guy
authors.initials: G
authors.lastname: Warnier
authors.affiliation: Ludwig Institute for Cancer Research, Brussels Branch, Belgium.|de Duve Institute, Université catholique de Louvain, Brussels, Belgium.
authors.forename: Magali
authors.initials: M
authors.lastname: de Heusch
authors.affiliation: INEM-UMR7355, Molecular Immunology, University of Orleans, Orleans, France.|CNRS, UMR7355 and Artimmune SAS, Orleans, France.
authors.forename: Dieudonnée
authors.initials: D
authors.lastname: Togbe
authors.affiliation: INEM-UMR7355, Molecular Immunology, University of Orleans, Orleans, France.|CNRS, UMR7355 and Artimmune SAS, Orleans, France.
authors.forename: Bernhard
authors.initials: B
authors.lastname: Ryffel
authors.affiliation: de Duve Institute, Université catholique de Louvain, Brussels, Belgium.
authors.forename: Pierre G
authors.initials: PG
authors.lastname: Coulie
authors.affiliation: Ludwig Institute for Cancer Research, Brussels Branch, Belgium.|de Duve Institute, Université catholique de Louvain, Brussels, Belgium.
authors.forename: Jean-Christophe
authors.initials: JC
authors.lastname: Renauld
authors.affiliation: Ludwig Institute for Cancer Research, Brussels Branch, Belgium.|de Duve Institute, Université catholique de Louvain, Brussels, Belgium.
authors.forename: Laure
authors.initials: L
authors.lastname: Dumoutier
mesh_terms: D000634:Aminoquinolines / Q000009:adverse effects*; D000818:Animals; D049109:Cell Proliferation; D002633:Chemotaxis / Q000235:genetics / Q000276:immunology*; D004195:Disease Models, Animal; D000077271:Imiquimod; D007113:Immunity, Innate / Q000235:genetics / Q000276:immunology; D007378:Interleukins / Q000096:biosynthesis* / Q000235:genetics; D051379:Mice; D018345:Mice, Knockout; D011565:Psoriasis / Q000209:etiology* / Q000378:metabolism* / Q000473:pathology; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000235:genetics / Q000378:metabolism; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000235:genetics / Q000378:metabolism; D018336:Receptors, Aryl Hydrocarbon / Q000172:deficiency / Q000235:genetics / Q000378:metabolism*; D016176:T-Lymphocyte Subsets / Q000276:immunology / Q000378:metabolism; D058504:Th17 Cells / Q000276:immunology / Q000378:metabolism; D000097043:Interleukin-22
chemical_list: D000634:Aminoquinolines; D000077271:Imiquimod; D007378:Interleukins; D016693:Receptors, Antigen, T-Cell, alpha-beta; D016692:Receptors, Antigen, T-Cell, gamma-delta; D018336:Receptors, Aryl Hydrocarbon; D000097043:Interleukin-22
keywords: AhR; IL-22; Imiquimod; Innate lymphoid cells (ILCs); Skin; T cells