Only in recent years, attentions have been drawn to the significance of expressing killer cell inhibitory receptors (KIR) in T cells KIRs specifically bind to the corresponding region of the MHC class I molecules and ...Only in recent years, attentions have been drawn to the significance of expressing killer cell inhibitory receptors (KIR) in T cells KIRs specifically bind to the corresponding region of the MHC class I molecules and transmit negative signals to prevent cytotoxity of T cells. When the ligands of KIRs are missing, the lysis of the target cells can’t be avoided. Perhaps the existence of KIRs is the main mechanism for preventing T cells from attacking autologous tissues. The recognition mechanism of the interaction between the KIR + donor T cells and the recipient’s MHC class I molecule expressing tissue cells might shed light on the establishment of the immunotolerance for the prevention of allo-graft rejection and graft-versus-host disease.展开更多
目的探讨溶血磷脂酸(lysophosphatidic acid,LPA)对人肺成纤维细胞(HFL-1)白细胞介素-13受体α2(IL-13Rα2)表达和Ⅰ型胶原(collagen typeⅠ,COLAⅠ)合成的影响。方法细胞培养,显微镜观察LPA对HFL-1细胞生长的影响,提取HFL-1细胞总RNA,...目的探讨溶血磷脂酸(lysophosphatidic acid,LPA)对人肺成纤维细胞(HFL-1)白细胞介素-13受体α2(IL-13Rα2)表达和Ⅰ型胶原(collagen typeⅠ,COLAⅠ)合成的影响。方法细胞培养,显微镜观察LPA对HFL-1细胞生长的影响,提取HFL-1细胞总RNA,用RT-PCR检测LPA对HFL-1细胞IL-13Rα2 mRNA和COLA I mRNA表达的影响。用免疫组化方法检测LPA和白细胞介素-13(interleukin-13,IL-13)对HFL-1细胞COLA I蛋白表达的影响。图像分析RT-PCR电泳条带和免疫组化图像,统计学处理。结果①LPA诱导HFL-1细胞IL-13Rα2 mRNA的表达,并呈时间依赖性。②1μmol.L-1 LPA刺激HFL-1细胞,IL-13Rα2 mR-NA的表达增强。③LPA作用HFL-1细胞,对IL-13Rα1的表达无影响。④LPA抑制HFL-1细胞COLA I mRNA的表达,IL-13促进COLA I mRNA的表达,LPA+IL-13混合组COLA I mRNA表达水平比LPA组高,比IL-13组低。⑤免疫组化结果与RT-PCR结果一致。结论溶血磷脂酸诱导人肺成纤维细胞表达IL-13 Rα2 mRNA,并下调人肺成纤维细胞合成COLAⅠ。展开更多
基金国家自然科学基金资助项目 (No .30 1 70 395)中国博士后科学基金资助项目 (No .2 0 0 1 - 2 9)
文摘Only in recent years, attentions have been drawn to the significance of expressing killer cell inhibitory receptors (KIR) in T cells KIRs specifically bind to the corresponding region of the MHC class I molecules and transmit negative signals to prevent cytotoxity of T cells. When the ligands of KIRs are missing, the lysis of the target cells can’t be avoided. Perhaps the existence of KIRs is the main mechanism for preventing T cells from attacking autologous tissues. The recognition mechanism of the interaction between the KIR + donor T cells and the recipient’s MHC class I molecule expressing tissue cells might shed light on the establishment of the immunotolerance for the prevention of allo-graft rejection and graft-versus-host disease.
文摘目的探讨溶血磷脂酸(lysophosphatidic acid,LPA)对人肺成纤维细胞(HFL-1)白细胞介素-13受体α2(IL-13Rα2)表达和Ⅰ型胶原(collagen typeⅠ,COLAⅠ)合成的影响。方法细胞培养,显微镜观察LPA对HFL-1细胞生长的影响,提取HFL-1细胞总RNA,用RT-PCR检测LPA对HFL-1细胞IL-13Rα2 mRNA和COLA I mRNA表达的影响。用免疫组化方法检测LPA和白细胞介素-13(interleukin-13,IL-13)对HFL-1细胞COLA I蛋白表达的影响。图像分析RT-PCR电泳条带和免疫组化图像,统计学处理。结果①LPA诱导HFL-1细胞IL-13Rα2 mRNA的表达,并呈时间依赖性。②1μmol.L-1 LPA刺激HFL-1细胞,IL-13Rα2 mR-NA的表达增强。③LPA作用HFL-1细胞,对IL-13Rα1的表达无影响。④LPA抑制HFL-1细胞COLA I mRNA的表达,IL-13促进COLA I mRNA的表达,LPA+IL-13混合组COLA I mRNA表达水平比LPA组高,比IL-13组低。⑤免疫组化结果与RT-PCR结果一致。结论溶血磷脂酸诱导人肺成纤维细胞表达IL-13 Rα2 mRNA,并下调人肺成纤维细胞合成COLAⅠ。
