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The role of macrophage reprogramming induced by GRA15II a polypeptide effector molecule of Toxoplasma gondii in liver diseases in model mice

机译:巨噬细胞重新编程诱导的弓形虫术治疗模型小鼠肝脏疾病中的多肽效应分子诱导的巨噬细胞重新编程

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摘要

GRA15II, a polypeptide effector molecule of T. gondii, binds TRAF6 to upregulate NF-κB signaling in macrophages and inhibits the proliferation and migration of tumor cells. a Treatment with GRA15II resulted in reprogramming of M2-like TAMs to the M1-like phenotype in nude mice. b Volcano plot indicating the genes that were differentially expressed (red, upregulated genes; green, downregulated genes in the GRA15 injection group relative to the vector group) in a microarray analysis of tumor samples from GRA15II and vector group mice. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis data showing the potential upstream regulators of the DEGs. c Coimmunoprecipitation of LV-gra15II- Mφ with proteins of the TNFR1, IL-1R, and TLR4 receptor complexes. Bound proteins were eluted and separated by SDS-PAGE and analyzed by western blotting using an anti-FLAG antibody and specific monoclonal antibodies against MyD88, IRAK1, TRAF6, and RIP1. GAPDH served as a control. For all statistical results, the data are shown as the mean ± SD. *P < 0.05, **P < 0.01; n.s. not significant; one-way ANOVA or two-tailed Student’s t test
机译:GRA15II是T.Gondii的多肽效应分子结合TRAF6以上调巨噬细胞中的NF-κB信号,并抑制肿瘤细胞的增殖和迁移。用GRA15II治疗导致M2样TAMS重新编程到裸鼠中的M1样表型。 B Volcano图表明差异表达的基因(红色,上调基因; GRA15注射组中的绿色,下调基因相对于载体组),在GRA15II和载体组小鼠的肿瘤样品的微阵列分析中。京都基因和基因组(Kegg)途径分析数据显示潜在上游调节器的途径。 C与TNFR1,IL-1R和TLR4受体复合物的蛋白质的LV-Gra15ii-mφ的C coimmunopectipitipitipitipitipitipitipitipipipipipipipipipipipipipipitipitipitipitipitipitipitipitipitipitipitation。用SDS-PAGE洗脱并分离结合的蛋白质,并使用抗标绳抗体和针对MyD88,Irak1,Traf6和RIP1的特异性单克隆抗体进行蛋白质印迹分析。 GAPDH作为一个控制。对于所有统计结果,数据显示为平均值±SD。 * P <0.05,** P <0.01; N.S.不重要;单向ANOVA或双尾学生的T测试

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