摘要
Irradiation-induced impaired gamma interferon(IFN-γ) production promotes tumor development and facilitates tumor relapse. Here, we sought to identify the characteristics of IFN-γ-secreting T and NK cells in response to single low-dose total-body irradiation(SLTBI) and also to highlight the role of rehmannia glutinosa(RG) on these cells during the process of recovery from irradiation-induced IFN-γ reduction. All IFN-γ-producing T and NK cells and signaling requirements(MHC-I, MHC-II, CD80,CD86) for Th1/Tc1 proliferation were determined by flow cytometry;the cytokine milieu(IL-12, IL-15, IL-2 etc.) that supports IFN-γ-secreting T and NK cells proliferations and the master transcription factor(T-bet) were detected by RT-PCR assay. The effect of RG on efficient IFN-γ production was confirmed in a lung melanoma metastasis model in irradiated mice. Our data showed that IFN-γ production by T and NK cells was significantly decreased after irradiation. IFN-γ-producing T cells subsets were more sensitive to irradiation injury than NK cells. Decreased nave T cells, reduced signaling from MHC molecular, CD80, CD86 and weakened cytokine support mainly contributed to the severe impaired IFN-γ-secreting T cells(Th1 and Tc1). However, the production of IFN-γ and the transcriptions of IL-12, IL-15, T-bet were obviously increased in RG-treated mice after irradiation(P<0.05). Therapy using RG elicited a remarkable proliferation of Tc1 and NK1 cells, which were necessary for the antitumor effect; and this efficacy of RG was confirmed in lung metastasis tumor model in RG-treated irradiated mice. Taken together, IFN-γ-secreting T cells exhibited a far greater sensitivity to irradiation-induced injury than NK cells. The promotion of RG on cellular basis of IFN-γ production by T and NK cells strengthened the anti-tumor immunity post SLTBI.
Irradiation-induced impaired gamma interferon(IFN-γ) production promotes tumor development and facilitates tumor relapse. Here, we sought to identify the characteristics of IFN-γ-secreting T and NK cells in response to single low-dose total-body irradiation(SLTBI) and also to highlight the role of rehmannia glutinosa(RG) on these cells during the process of recovery from irradiation-induced IFN-γ reduction. All IFN-γ-producing T and NK cells and signaling requirements(MHC-I, MHC-II, CD80,CD86) for Th1/Tc1 proliferation were determined by flow cytometry;the cytokine milieu(IL-12, IL-15, IL-2 etc.) that supports IFN-γ-secreting T and NK cells proliferations and the master transcription factor(T-bet) were detected by RT-PCR assay. The effect of RG on efficient IFN-γ production was confirmed in a lung melanoma metastasis model in irradiated mice. Our data showed that IFN-γ production by T and NK cells was significantly decreased after irradiation. IFN-γ-producing T cells subsets were more sensitive to irradiation injury than NK cells. Decreased nave T cells, reduced signaling from MHC molecular, CD80, CD86 and weakened cytokine support mainly contributed to the severe impaired IFN-γ-secreting T cells(Th1 and Tc1). However, the production of IFN-γ and the transcriptions of IL-12, IL-15, T-bet were obviously increased in RG-treated mice after irradiation(P<0.05). Therapy using RG elicited a remarkable proliferation of Tc1 and NK1 cells, which were necessary for the antitumor effect; and this efficacy of RG was confirmed in lung metastasis tumor model in RG-treated irradiated mice. Taken together, IFN-γ-secreting T cells exhibited a far greater sensitivity to irradiation-induced injury than NK cells. The promotion of RG on cellular basis of IFN-γ production by T and NK cells strengthened the anti-tumor immunity post SLTBI.
引文