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作 者:方廖琼[1] 傅晓岚[2] 牛荣[3] 纪贤文[3] 魏泓[3]
机构地区:[1]西南大学生物技术学院,重庆400715 [2]第三军医大学基础医学部全军免疫学研究所,重庆400038 [3]第三军医大学基础医学部动物学教研室,重庆400038
出 处:《中国病理生理杂志》2008年第9期1845-1849,共5页Chinese Journal of Pathophysiology
基 金:重庆市教育委员会资助项目(No.KJ070616)
摘 要:目的:分析羊胎盘免疫调节因子(GPIF)对BALB/c小鼠T淋巴细胞共刺激表面抗原分子表达及其细胞因子分泌的影响,探讨羊胎盘免疫调节因子免疫促进作用机理。方法:60Coγ-ray辐射所致免疫抑制小鼠连续7 d腹腔注射GPIF,流式细胞分析术分析BALB/c小鼠脾细胞表达CD28+、CD152+单阳性细胞百分率,表达CD4+CD28+、CD8+CD28+、CD4+CD152+、CD8+CD152+双阳性细胞百分率;ELISA法检测小鼠血清IL-2、IFN-γ分泌水平。结果:羊胎盘免疫调节因子显著提高免疫损伤小鼠脾淋巴细胞CD28+、CD4+CD28+、CD8+CD28+阳性细胞百分率(P<0.05,P<0.01),降低CD152+、CD4+CD152+阳性细胞百分率(P<0.05,P<0.01),提高小鼠血清IL-2、IFN-γ分泌水平(P<0.01)。结论:羊胎盘免疫调节因子的免疫促进作用与其调节T淋巴细胞CD28、CD152共刺激分子通路的活化信号传递,降低T淋巴细胞的功能抑制,促进T淋巴细胞的活化有关。活化的T淋巴细胞分泌细胞因子IL-2、IFN-γ,参与细胞因子介导的免疫网络调节。AIM: To investigate the effects of goat placenta immunoregulating factor (GPIF) on the expression of costimulatory molecules lineaged T cells in BALB/c mice. METHODS: Animal model for immunodeficiency made from BALB/c mice with whole - body irradiation by 5 Gy ^60Coγ-ray was applied for research. The immunosuppressive mice were injected with GPIF for seven days continuously: FACS was applied to analyze the rate of CD28^+, CD152^+ , CD4^+ CD28 ^+ , CD8 ^+ CD28 ^+ , CD4 ^+ CD152 ^+ and CD8 ^+ CD152 ^+ cells in splenic lymphocytes and ELISA method was employed to measure the amount of IL - 2 and IFN - γ in serum of mice. RESULTS : GPIF increased the percentage of CD28 ^+ , CD4 ^+ CD28 ^+ and CD8 ^+ CD28 ^+ cells ( P 〈 0. 05, P 〈 0. 01 ), and decreased the percentage of CD152 ^+ ( P 〈 0. 05, P 〈 0. 01 ), CD4 ^+ CD152 ^+ cells (P 〈0. 05, P 〈0. 01 ) in splenic lymphocytes of immunosuppressive mice significantly. GPIF increased the content of IL- 2 and IFN- γ in serum of mice simultaneously (P 〈 0.01 ). CONCLUSION: Immuno- enhancing effect of GPIF facilitates the costimulation of CD28 pathway, which can activate T cells and accelerate the course of renewing T cell activity. The function of GPIF may have close relationship with an immune network formed by the secretion of IL -2 and IFN -γ and the expression of CD28 and CD152.
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