Fiorillo M T, Toniatti C, Van Snick J, Ciliberto G
Istituto Ricerche Biologia Molecolare, Roma, Italy.
Eur J Immunol. 1992 Mar;22(3):799-804. doi: 10.1002/eji.1830220325.
This paper reports on cDNA coding for the 80-kDa murine IL6 receptor (mIL6R) that was cloned from a mouse liver cDNA library. Human hepatoma Hep3B cells transfected transiently or stably with an expression vector carrying the entire coding region for mIL6R become responsive to mouse IL6 (mIL6). We monitored response to the cytokine through the transcriptional activation of a co-transfected IL6-inducible human C-reactive protein (CRP) promoter; response to mIL6 is lost upon treatment of the cells with increasing amounts of a monoclonal antibody to mIL6R. mIL6R mutants have been generated in the carboxy-terminal portion of the molecule. Their functional analysis in hepatoma cells shows that the intracytoplasmic domain of the receptor is not absolutely essential to IL6 signal transduction (i.e. CRP promoter activation), but that the last 40 amino acids contribute to maximal IL6 response in these cells.
本文报道了从小鼠肝脏cDNA文库中克隆出的编码80kDa小鼠IL6受体（mIL6R）的cDNA。用携带mIL6R完整编码区的表达载体瞬时或稳定转染的人肝癌Hep3B细胞对小鼠IL6（mIL6）产生反应。我们通过共转染的IL6诱导型人C反应蛋白（CRP）启动子的转录激活来监测对细胞因子的反应；用越来越多的抗mIL6R单克隆抗体处理细胞后，对mIL6的反应丧失。已在该分子的羧基末端部分产生了mIL6R突变体。它们在肝癌细胞中的功能分析表明，受体的胞质内结构域对于IL6信号转导（即CRP启动子激活）并非绝对必要，但最后40个氨基酸有助于这些细胞中最大程度的IL6反应。
