Research paperTGF-β1 improving abnormal pregnancy outcomes induced by Toxoplasma gondii infection: Regulating NKG2D/DAP10 and killer subset of decidual NK cells

- 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.