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Xu, Xiaoyan; Zhang, Jian; Zhan, Shaowei; Li, Zhidan; Liu, Xianbing; Zhang, Haixia; Jiang, Yuzhu; Hu, Xuemei
Cellular immunology, July 2017, 2017-Jul, 2017-07-00, 20170701, Volume: 317Journal Article
•Improved pregnancy outcomes were observed after TGF-β1 treatment following T. gondii infection.•TGF-β1 could down-regulate the expression of NKG2D/DAP10 of dNK cells induced by T. gondii infection.•TGF-β1 could down-regulate the ratio of killer subset of dNK cells induced by T. gondii infection.•TGF-β1 could decrease the cytotoxicity of dNK cells caused by T. gondii infection. Our current aim was to investigate whether injection of TGF-β1 played an important role in improving abnormal pregnancy outcomes with T. gondii infection and how the TGF-β1 regulated. Results showed that TGF-β1 exhibited improved pregnancy outcomes induced by T. gondii infection. dNK cytotoxicity was increased with T. gondii infection while decreased with TGF-β1 treatment. dNK cytotoxicity related NKG2D/DAP10 expression, perforin, granzyme, IFN-γ and killer subsets were all increased with T. gondii infection while decreased after TGF-β1 treatment. In addition, anti-TGF-β1 antibodies could aggregate the cytotoxicity of dNK cells and the levels of molecules above. These results indicated that TGF-β1 treatment could improve the abnormal pregnancy outcomes with T. gondii infection by decreasing the cytotoxicity of dNK cells mediated by NKG2D/DAP10 pathway and killer subset. These results suggested that TGF-β1 might be a potential immunoprotective method for the treatment of abnormal pregnancy outcomes following T. gondii infection.
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