| First Author | Cochez PM | Year | 2017 |
| Journal | J Invest Dermatol | Volume | 137 |
| Issue | 5 | Pages | 1094-1103 |
| PubMed ID | 28115058 | Mgi Jnum | J:240880 |
| Mgi Id | MGI:5896685 | Doi | 10.1016/j.jid.2016.12.023 |
| Citation | Cochez PM, et al. (2017) Ccr6 Is Dispensable for the Development of Skin Lesions Induced by Imiquimod despite its Effect on Epidermal Homing of IL-22-Producing Cells. J Invest Dermatol 137(5):1094-1103 |
| abstractText | Expression of the chemokine receptor Ccr6 is shared by most IL-22-producing cells, and Ccr6-deficient mice showed decreased IL-22 production and skin inflammation upon IL-23 intradermal injections. To determine whether this observation might be extended to another psoriasis model, we applied imiquimod on Ccr6-deficient mice. Although epidermal IL-22 production was decreased because of a deficient recruitment of gammadelta T cells in these mice, they were not protected against psoriatic lesions. When primary epidermis or dermis tissue culture cells from nontreated mice were stimulated ex vivo with IL-1alpha/IL-2/IL-23, we observed that Ccr6 is crucial for Il22 expression from epidermal but not dermal cultures. Taking advantage of Ccr6-LacZ-knock-in mice, we showed that Ccr6 is necessary for the homing of Ccr6-positive cells, probably a gammadelta T-cell subset, which represents the main potential IL-22 source in the epidermis. Similar results were observed in Rag1-/- epidermis and dermis primary cultures, in which a subset of innate lymphoid cells expressing Ccr6 represents the main potential source of IL-22. Taken together, our data show that Ccr6 is not required for the development of skin lesions induced by imiquimod despite its effect on epidermal homing of IL-22-producing cells. |
