| First Author | Tanaka R | Year | 2022 |
| Journal | J Invest Dermatol | PubMed ID | 35803322 |
| Mgi Jnum | J:328267 | Mgi Id | MGI:7334594 |
| Doi | 10.1016/j.jid.2022.06.006 | Citation | Tanaka R, et al. (2022) The Role of PD-L1 on Langerhans Cells in the Regulation of Psoriasis. J Invest Dermatol |
| abstractText | Langerhans cells (LCs) are skin-resident cells with potent antigen-presenting cell capabilities, which reportedly play some roles in the development of psoriasis, an inflammatory skin disease mediated by IL-17Aproducing cells, T helper 17 cells, and TCR-gammadelta(low) T cells. LCs in psoriatic skin lesions but not in normal skin express PD-L1, which binds to PD-1, an immune checkpoint molecule, to negatively regulate immune reactions. The aim of this study is to elucidate the regulatory role of LCs through the PD-1/PD-L1 axis in a murine model of imiquimod-induced psoriasis-like dermatitis. Imiquimod application on wild-type C57BL/6J mice induced PD-L1 expression on LCs both in the ear skin and skin-draining lymph nodes. To further identify the functional role of PD-L1 expressed on LCs, we generated conditional knockout mice lacking PD-L1 expression on LCs (Pd-l1-cKO mice). Pd-l1-cKO mice presented significantly more severe imiquimod-induced psoriasis-like dermatitis than their control littermates. Flow cytometric analysis showed that the frequency of activated IL-17Aproducing gammadelta(low) T cells was increased in the ear skin samples, and IL-17A production by CCR6(+) migrating gammadelta(low) T cells increased in the skin-draining lymph nodes in imiquimod-applied Pd-l1-cKO mice than in control littermates. Collectively, LCs disrupt the exacerbation of psoriasis through PD-L1. |
