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Publication : Costimulatory Molecule CD226 Regulates Atopic Dermatitis in a Mouse Model.

First Author  Qiao W Year  2024
Journal  J Invest Dermatol PubMed ID  38325579
Mgi Jnum  J:346403 Mgi Id  MGI:7616152
Doi  10.1016/j.jid.2024.01.022 Citation  Qiao W, et al. (2024) Costimulatory Molecule CD226 Regulates Atopic Dermatitis in a Mouse Model. J Invest Dermatol
abstractText  This study investigated the role of CD226 in a 2,4-dinitrochlorobenzene (DNCB)-induced mouse model of atopic dermatitis. The results showed that the lack of CD226 (global and CD4(+) T-cell specific) significantly increased ear thickness, reddening, swelling, and scaling of the skin as well as inflammatory cell and mast cell infiltration. RT-qPCR results demonstrated that the mRNA expressions of atopic dermatitis-related inflammatory cytokines and chemokines were markedly increased in the draining lymph nodes and lesioned ear skin tissues of global and CD4(+) T-cell-specific CD226-deficient mice compared with that in control mice. In vitro assessment revealed that CD226 directly modulates TGFbeta-mediated regulatory T (Treg) cell differentiation and proliferation. Notably, Treg cell-specific deletion of CD226 (Cd226(fl/fl)Foxp3(cre) mice) resulted in more severe dermatitis and epidermal thickening than those observed in littermate mice upon DNCB treatment. Subsequent analysis showed that the infiltration of Treg cells in ear lesions and the number of Tregs in the spleen were significantly reduced in Cd226(fl/fl)Foxp3(cre) mice after DNCB treatment. In addition, the lack of CD226 induced apoptosis of Treg cells through the activation of caspase 3. Therefore, these results suggest that CD226 has potential efficacy in atopic dermatitis, correlating with Treg cell inhibition.
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