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目的观察脂多糖所致脓毒症小鼠树突状细胞GITRL表达及免疫功能的改变。方法以10 ng/mL脂多糖刺激体外诱导小鼠树突状细胞模拟脓毒症免疫麻痹体系,利用流式细胞术和Brd U细胞增殖反应试剂盒分别检测树突状细胞表面分子CD11c、CD80和GITRL表达、混合淋巴细胞增殖反应及CD4~+CD25~+Foxp3~+Treg水平。结果脂多糖引起树突状细胞标志分子CD11c、CD80和负调控分子GITRL的表达分别由6.97%、2.61%和22.39%增加到16.02%、13.35%和49.74%,差异均有统计学意义(P<0.01)。平均荧光密度值由4.81增加到17.95,差异有统计学意义(P<0.01)。然而抗原特异性混合淋巴细胞反应OD值由0.532减少为0.419,差异有统计学意义(P<0.01),并且GITRL激活的CD4~+CD25~+Foxp3~+Treg由5.71%增加到8.31%,差异有统计学意义(P<0.05)。结论脂多糖所致脓毒症小鼠树突状细胞表达高水平的免疫共抑制GITRL分子,通过GITRL-GITR激活Treg细胞抑制T细胞增殖和功能,引起免疫麻痹状态。
Objective To observe the changes of GITRL expression and immune function in dendritic cells induced by lipopolysaccharide in mice. Methods 10 ng / mL lipopolysaccharide was used to stimulate the dendritic cells induced by dendritic cells in vitro to simulate the sepsis immune paralysis system. Flow cytometry and BrdU proliferation assay were used to detect the expression of CD11c, CD80 and GITRL expression, mixed lymphocyte proliferation and CD4 ~ + CD25 ~ + Foxp3 ~ + Treg levels. Results The expression of dendritic cell marker molecules CD11c, CD80 and negative regulator GITRL increased from 6.97%, 2.61% and 22.39% to 16.02%, 13.35% and 49.74%, respectively, with statistical significance (P < 0.01). The average fluorescence density increased from 4.81 to 17.95, the difference was statistically significant (P <0.01). However, the OD value of antigen-specific mixed lymphocyte reaction decreased from 0.532 to 0.419 (P <0.01), and the GITRL-activated CD4 ~ + CD25 ~ + Foxp3 ~ + Treg increased from 5.71% to 8.31% There was statistical significance (P <0.05). Conclusions Dendritic cells induced by lipopolysaccharide in dendritic cells can express high levels of immunosuppressive GITRL molecules. GITRL-GITR can activate Treg cells to inhibit the proliferation and function of T cells and cause immune paralysis.