| First Author | Cochez PM | Year | 2016 |
| Journal | Eur J Immunol | Volume | 46 |
| Issue | 6 | Pages | 1449-59 |
| PubMed ID | 27000947 | Mgi Jnum | J:247182 |
| Mgi Id | MGI:5923581 | Doi | 10.1002/eji.201546070 |
| Citation | Cochez PM, et al. (2016) AhR modulates the IL-22-producing cell proliferation/recruitment in imiquimod-induced psoriasis mouse model. Eur J Immunol 46(6):1449-59 |
| abstractText | 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: gammadelta T cells, Th17 cells, and ILC3, and a novel IL-22-producing cell type identified in this setting: CD4(-) CD8(-) TCRbeta(+) 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 gammadelta T cells, ILC3, and CD4(-) CD8(-) TCRbeta(+) 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 gammadelta T cells, CD4(-) CD8(-) TCRbeta(+) T cells and ILCs. |
