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J Invest Dermatol. 2017 May;137(5):1094-1103. doi: 10.1016/j.jid.2016.12.023. Epub 2017 Jan 20.

Ccr6 Is Dispensable for the Development of Skin Lesions Induced by Imiquimod despite its Effect on Epidermal Homing of IL-22-Producing Cells.

Author information

1
Ludwig Institute for Cancer Research, Brussels Branch, Brussels, Belgium; de Duve Institute, Université catholique de Louvain, Brussels, Belgium.
2
de Duve Institute, Université catholique de Louvain, Brussels, Belgium.
3
Ludwig Institute for Cancer Research, Brussels Branch, Brussels, Belgium.
4
Ludwig Institute for Cancer Research, Brussels Branch, Brussels, Belgium; de Duve Institute, Université catholique de Louvain, Brussels, Belgium. Electronic address: laure.dumoutier@uclouvain.be.

Abstract

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 γδ 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-1α/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 γδ 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.

PMID:
28115058
DOI:
10.1016/j.jid.2016.12.023
[Indexed for MEDLINE]
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