CD4+CD25+调节性T细胞对氧化型低密度脂蛋白活化的巨噬细胞功能的影响

目的 研究CD4+CD25+调节性T细胞对氧化型低密度脂蛋白(oxLDL)激活的巨噬细胞功能的影响及其机制.方法 磁性细胞分离器(MACS)分离CD4+CD25+T细胞及CD4+CD25-T细胞,在oxLDL作用下,将巨噬细胞分别与CD4+CD25+T细胞、CD4+CD25-T细胞共培养48 h.采用流式细胞术检测巨噬细胞HLA-DR、CD86的表达;ELISA检测上清液MCP-1、MMP-9、TNF-α、TGF-β和IL-10细胞因子的表达;采用Griess反应测定NO生成量,RT-PCR测定iNOS表达.结果 与对照组比较,CD4+CD25+T细胞可显著抑制oxLDL激活的巨噬细胞HLA-DR及CD86的表达、减少NO生成、抑制iNOS mRNA表达和促炎细胞因子生成.结论 调节性T细胞可促使oxLDL激活的巨噬细胞由具有促炎表型的M1型向具有抗炎表型的M2型转化.

Modulation of macrophage function stimulated with oxidized low density lipoprotein by CD4+CD25+regulatory T cells

Objective To investigate whether and how CD4 + CD25 + regulatory T cells(Tr) affect oxidized low density lipoprotein(oxLDL) induced proinflammatory response in macrophages.Methods Tr were isolated from lymphocyte suspensions by magnetic cell sorting-column and analyzed by flow cytometry.Macrophages were cultured alone,with CD4 + CD25 + Tr or CD4 + CD25 - Tr in the presence of oxLDL for 48 h.The phenotype of macrophages was determined by flow cytometry.NO production was assessed by Griess reaction an iNOS mRNA was isolated by RT-PCR.ELISA were used to measure the production of cytokine/chemokine like MCP-1,MMP-9,TNF-ct,TGF-β and IL-10 in macrophages response to oxLDL.Results Our data showed that with oxLDL challenge,the Tr modulated macrophages have decreased NO production and iNOS expression,decreased HLA-DR and CD86 expression,and down-regulated proinflammatory cytokine/chemokine production.Conclusion Tr can inhibit the proinflammatory properties of macrophages and steer macrophage differentiation toward an anti-inflammatory cytokine producing phenotype.