Human dental pulp stem cells ameliorate the imiquimod-induced psoriasis in mice
Kang Wen,
Wu Li,
Chen Cheng,
Xie Weige,
Chen Jiaqi,
Song Shiyu,
Huang Lingyan,
Wang Hongwei,
Xie Sijing
Affiliations
Kang Wen
Department of Endodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, 210008, China
Wu Li
Department of Endodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, 210008, China
Chen Cheng
Department of Endodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, 210008, China
Xie Weige
Department of Endodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, 210008, China
Chen Jiaqi
Department of Endodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, 210008, China
Song Shiyu
State Key Laboratory of Analytical Chemistry for Life Science and Jiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing University, Nanjing, 210093, China
Huang Lingyan
Department of Endodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, 210008, China
Wang Hongwei
State Key Laboratory of Analytical Chemistry for Life Science and Jiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing University, Nanjing, 210093, China; Corresponding author.
Xie Sijing
Department of Endodontics, Nanjing Stomatological Hospital, Medical School of Nanjing University, Nanjing, 210008, China; Corresponding author.
Psoriasis is an autoimmune disease, which has a significant impact on the quality of patient’s life. And, there is still no cure for psoriasis. The human dental pulp stem cell (hDPSC) possesses the properties of immunoregulation. In this study, we aimed to determine the effect of hDPSC on the imiquimod (IMQ)-induced psoriasis in mice. The psoriasis model was established by topical application of IMQ cream in mice for 7 days. We found that subcutaneous injection of hDPSC could reduce the symptoms of skin lesions in IMQ-induced psoriasis and suppress the expression of keratin 16, S100A8, S100A9, which are associated with abnormal epidermal proliferation. Subepithelial inflammatory cytokines, CD4+ T lymphocytes and CD11c+ dendritic cells infiltrations were significantly inhibited in by hDPSC. The TNF-α, IFN-γ expressions in serum were decreased, and splenomegaly induced by IMQ was improved after hDPSC treatment. In summary, our study demonstrated that hDPSC could reduce the symptoms of skin lesions and suppress local and systemic immune responses of IMQ-induced psoriasis in mice, which might provide a new sight for the treatment of psoriasis.