Cellular basis of Impaired IFN-γ Production after Single Lowdose Total-Body Irradiation and Protection of Rehmannia Glutinosa
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- 英文论文题名：Cellular basis of Impaired IFN-γ Production after Single Lowdose Total-Body Irradiation and Protection of Rehmannia Glutinosa
- 论文作者：An Lei ; Guo Yuqi ; Sun Xiaoyan ; Wang Li ; Zhou Xianbin ; Lv Yanmin ; Yao Chengfang
- 英文论文作者：An Lei ; Guo Yuqi ; Sun Xiaoyan ; Wang Li ; Zhou Xianbin ; Lv Yanmin ; Yao Chengfang ; Key Laboratory for Tumor Immunology and Traditional Chinese Medicine Immunology ; Institute of Basic Medicine ; Shandong Academy of Medical Sciences ; School of Medicine and Life Science ; University of Jinan-Shandong Academy of Medical Science
- 年：2016
- 作者机构：Key Laboratory for Tumor Immunology and Traditional Chinese Medicine Immunology,Institute of Basic Medicine,Shandong Academy of Medical Sciences;School of Medicine and Life Science,University of Jinan-Shandong Academy of Medical Science;
- 英文论文关键词：IFN-γ ; CD4+T ; CD8+T ; NK ; Rehmannia glutinosa ; irradiation
- 会议召开时间：2016-11-04
- 会议录名称：第十一届全国免疫学学术大会摘要汇编
- 英文会议录名称：Abstracts of 2016 CSI Congress on Immunology
- 语种：英文
- 分类号：R730.55
- 学会代码：IGMD
- 会议名称：第十一届全国免疫学学术大会
- 会议地点：中国安徽合肥
- 主办单位：中国免疫学会
- 学会名称：中国免疫学会
- 页数：1
- 文件大小：1302k
- 原文格式：D
- 会议级别：全国
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.
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.
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