HSP60特异性调节性T细胞的诱导及其对小鼠动脉粥样硬化影响
发布时间：2019-01-01 20:53
【摘要】： ApoE-/-小鼠CD4+CD25+ T细胞分离及功能检测 目的探讨ApoE-/-小鼠CD4+CD25+T细胞的比例和功能及其与动脉粥样硬化的关系。方法从apoE-/-小鼠外周血流式细胞仪(FCA)检测CD4+CD25+T细胞的比例并分分选之;混合淋巴细胞反应(MLR)研究CD4+CD25+T细胞的免疫抑制功能;ELISA法测定上清液中细胞因子IL-10、TGF-β浓度;观察ApoE-/-小鼠动脉粥样斑块的形成状况。结果与正常小鼠相比,ApoE-/-小鼠外周血中CD4+CD25+T细胞数量无差异,但抑制naive T细胞增殖能力弱,分泌更少IL-10、TGF-β;ApoE-/-小鼠斑块面积较大。结论ApoE-/-小鼠CD4+CD25+T细胞抑制功能弱,可能因此免疫失稳而致动脉粥样硬化。 HSP60特异性调节性T细胞的诱导及其对小鼠动脉粥样硬化影响 目的探讨抗原特异性CD4+CD25+T细胞的体外诱导及其对动脉粥样硬化斑块形成的影响。方法从apoE-/-小鼠分离骨髓单个核细胞,经雷帕霉素(RPM)处理培养出未成熟树突状细胞(DC);体外诱导HSP60特异性调节性T细胞分化;流式细胞仪(FCA)检测及分选CD4+CD25+T细胞;混合淋巴细胞反应(MLR)研究CD4+CD25+T细胞的特异性抑制效应;ELISA法测定上清液中细胞因子IL-10、TGF-β和IFN-γ浓度。过继转移CD4+CD25+T细胞后,观察小鼠动脉粥样斑块的形成状况。结果雷帕霉素处理的DC共刺激分子CD80和CD86表达明显减少,形态学表现为未成熟树突状细胞;未成熟树突状细胞比成熟树突状细胞能诱导更多CD4+CD25+T细胞;培养体系中细胞因子IL-10、TGF-β水平明显升高;CD4+CD25+T细胞能抑制效应性T细胞的增殖及IFN-γ的分泌。过继HSP60特异性CD4+CD25+T细胞组小鼠斑块面积较小。结论未成熟树突状细胞可诱导出抑制功能强大的HSP60特异性CD4+CD25+T细胞,后者在体内能能明显抑制斑块的形成。
[Abstract]:Isolation and functional determination of CD4 CD25 T cells in ApoE-/- mice objective to investigate the proportion and function of CD4 CD25 T cells in ApoE-/- mice and their relationship with atherosclerosis. Methods the proportion of CD4 CD25 T cells was detected by flow cytometry (FCA) in peripheral blood of apoE-/- mice, and the immunosuppressive function of CD4 CD25 T cells was studied by mixed lymphocyte reaction (MLR). The concentration of cytokine IL-10,TGF- 尾 in supernatant was determined by ELISA method, and the formation of atherosclerotic plaques in ApoE-/- mice was observed. Results compared with normal mice, the number of CD4 CD25 T cells in peripheral blood of ApoE-/- mice was not different, but the ability of inhibiting the proliferation of naive T cells was weak, and the secretion of IL-10,TGF- 尾 was less, and the plaque area of ApoE-/- mice was larger. Conclusion the inhibitory function of CD4 CD25 T cells in ApoE-/- mice is weak, which may result in atherosclerosis due to immune instability. Induction of HSP60 specific regulatory T cells and their effects on atherosclerosis in mice objective to investigate the induction of antigen-specific CD4 CD25 T cells in vitro and their effects on atherosclerotic plaque formation. Methods Bone marrow mononuclear cells were isolated from apoE-/- mice and immature dendritic cells (DC);) were cultured with rapamycin (RPM) to induce HSP60 specific regulatory T cell differentiation in vitro. The specific inhibitory effect of CD4 CD25 T cells was studied by mixed lymphocyte reaction (MLR), and the concentration of cytokines IL-10,TGF- 尾 and IFN- 纬 in supernatant was determined by ELISA assay. After adoptive transfer of CD4 CD25 T cells, the formation of atherosclerotic plaques in mice was observed. Results the expression of CD80 and CD86 in DC costimulatory molecules was significantly decreased after treatment with rapamycin, and the morphological features were immature dendritic cells, and immature dendritic cells could induce more CD4 CD25 T cells than mature dendritic cells. The level of cytokine IL-10,TGF- 尾 was significantly increased in culture system, and CD4 CD25 T cells could inhibit the proliferation of effectual T cells and the secretion of IFN- 纬. The plaque area of adoptive HSP60 specific CD4 CD25 T cell group was smaller. Conclusion immature dendritic cells can induce potent HSP60 specific CD4 CD25 T cells which can inhibit plaque formation in vivo.
【学位授予单位】：华中科技大学
【学位级别】：硕士
【学位授予年份】：2007
【分类号】：R392
本文编号：2398095
[Abstract]:Isolation and functional determination of CD4 CD25 T cells in ApoE-/- mice objective to investigate the proportion and function of CD4 CD25 T cells in ApoE-/- mice and their relationship with atherosclerosis. Methods the proportion of CD4 CD25 T cells was detected by flow cytometry (FCA) in peripheral blood of apoE-/- mice, and the immunosuppressive function of CD4 CD25 T cells was studied by mixed lymphocyte reaction (MLR). The concentration of cytokine IL-10,TGF- 尾 in supernatant was determined by ELISA method, and the formation of atherosclerotic plaques in ApoE-/- mice was observed. Results compared with normal mice, the number of CD4 CD25 T cells in peripheral blood of ApoE-/- mice was not different, but the ability of inhibiting the proliferation of naive T cells was weak, and the secretion of IL-10,TGF- 尾 was less, and the plaque area of ApoE-/- mice was larger. Conclusion the inhibitory function of CD4 CD25 T cells in ApoE-/- mice is weak, which may result in atherosclerosis due to immune instability. Induction of HSP60 specific regulatory T cells and their effects on atherosclerosis in mice objective to investigate the induction of antigen-specific CD4 CD25 T cells in vitro and their effects on atherosclerotic plaque formation. Methods Bone marrow mononuclear cells were isolated from apoE-/- mice and immature dendritic cells (DC);) were cultured with rapamycin (RPM) to induce HSP60 specific regulatory T cell differentiation in vitro. The specific inhibitory effect of CD4 CD25 T cells was studied by mixed lymphocyte reaction (MLR), and the concentration of cytokines IL-10,TGF- 尾 and IFN- 纬 in supernatant was determined by ELISA assay. After adoptive transfer of CD4 CD25 T cells, the formation of atherosclerotic plaques in mice was observed. Results the expression of CD80 and CD86 in DC costimulatory molecules was significantly decreased after treatment with rapamycin, and the morphological features were immature dendritic cells, and immature dendritic cells could induce more CD4 CD25 T cells than mature dendritic cells. The level of cytokine IL-10,TGF- 尾 was significantly increased in culture system, and CD4 CD25 T cells could inhibit the proliferation of effectual T cells and the secretion of IFN- 纬. The plaque area of adoptive HSP60 specific CD4 CD25 T cell group was smaller. Conclusion immature dendritic cells can induce potent HSP60 specific CD4 CD25 T cells which can inhibit plaque formation in vivo.
【学位授予单位】：华中科技大学
【学位级别】：硕士
【学位授予年份】：2007
【分类号】：R392
【参考文献】
相关期刊论文 前2条
1 朱建健,王宪;慢性炎症、自身免疫和动脉粥样硬化[J];生理科学进展;2002年04期
2 周军,汪建平,兰平,吴小剑,黄美近,宋新明;结肠抗原特异性T细胞克隆回输治疗大鼠溃疡性结肠炎的研究[J];中华实验外科杂志;2004年10期
，本文编号：2398095
本文链接：https://www.wllwen.com/yixuelunwen/binglixuelunwen/2398095.html
最近更新
教材专著
