髓性TGF-β受体Ⅱ敲除鼠的建立及其巨噬细胞表型的初步分析

A Phonotypic Analysis of Macrophages Derived from Myeloid TGF-β Receptor Ⅱ Knockout Mice

目的:建立髓性TGF-β受体II(TβRII)敲除鼠模型并对其巨噬细胞表型进行了初步分析。方法:利用溶菌酶M启动子-重组酶转基因鼠(lysozyme M-Cre鼠)和TβRII条件敲除鼠,建立定向髓性TβRII敲除鼠,通过基因型检测、免疫细胞的分布组成,然后检测敲除鼠巨噬细胞细胞因子表达的变化及对肿瘤细胞凋亡的影响。结果:建立了髓性TβRII敲除鼠,并初步证明,在肿瘤细胞上清刺激条件下,TβRII敲除的巨噬细胞与对照细胞相比,CXCL1表达量下调。结论:TGF-β信号可调控巨噬细胞的CXCL1表达。

Objective： To establish myeloid TGF-βreceptor I（ITβRII）-deficient mice and analyze the impact of TβRII deficiency on macrophages.Methods： Mice carrying the floxed allele of TβRII and lysozyme M-Cre were used for generation of mice with myeloid cell-specific deletion of TβRII.Mouse genotyping and distribution of immune cells in mice were examined.The effect of TβRII deletion on the cytokine expression by the macrophage was examined using real-time quantitative PCR.The apoptosis of tumor cells was examined by flow cytometry.Results： Myeloid TβRII knockout mice were generated;TβRII-deficient macrophages upon stimulation with the supernatants of the tumor cells,expressed lower levels of CXCL1 compared with control macrophages.Conclusions： TGF-β signaling can significantly regulate the expression of CXCL1 in macrophages.