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目的观察B7-H1信号在脂多糖(lipopoiysaccharide,LPS)所致脓毒症小鼠免疫麻痹中的作用。方法 2016年9月—2017年2月观察LPS刺激树突状细胞(dendritic cells,DCs)引起脓毒症免疫麻痹、DCs分化、B7-H1表达及抗原特异性T细胞增殖反应的变化,分别利用显微拍照技术、流式细胞分析术、免疫荧光技术和Brd U细胞增殖反应试剂盒检测。应用Graph Pad Prism 5统计分析,组间均数采用t检验或单因素方差分析Newman-Keuls检验。P<0.05为差异有统计学意义。结果 LPS促进树突状细胞分化成熟,且B7-H1表达阳性百分比由(4.65±1.29)%增加到(46.05±1.08)%,抗原提呈SIINFEKL-H2Kb百分比由(18.68±0.52)%上升到(90.54±0.44)%;但抗原特异性T淋巴细胞反应OD值由(0.747±0.085)减少为(0.368±0.050),封闭B7-H1信号OD值增加到(0.585±0.033),对比差异均有统计学意义(均P<0.05)。结论阻断免疫共抑制B7-H1信号可改善细菌所致脓毒症小鼠T细胞免疫反应低下的免疫麻痹状态。
Objective To observe the role of B7-H1 signaling in immune paralysis induced by lipopoiysaccharide (LPS) -induced sepsis in mice. Methods From September 2016 to February 2017, we observed the changes of dendritic cells (DCs) induced by LPS in sepsis, DCs differentiation, B7-H1 expression and antigen-specific T cell proliferation. Micrograph technique, flow cytometry, immunofluorescence and BrdU cell proliferation reaction kit. Using Graph Pad Prism 5 statistical analysis, the mean between groups using t test or one-way analysis of variance Newman-Keuls test. P <0.05 for the difference was statistically significant. Results LPS promoted dendritic cell differentiation and maturation, and the positive percentage of B7-H1 expression increased from (4.65 ± 1.29)% to (46.05 ± 1.08)%. The percentage of SIINFEKL-H2Kb antigen increased from (18.68 ± 0.52)% to 90.54 ± 0.44)%. However, the OD value of antigen-specific T lymphocyte reaction decreased from (0.747 ± 0.085) to (0.368 ± 0.050) and the value of blocked B7-H1 signal increased to (0.585 ± 0.033) Significance (both P <0.05). Conclusion Blocking the co-immunosuppression B7-H1 signal can improve immune paralysis of T-cell immune response in mice with bacterial-induced sepsis.