Chedid M, Shirakawa F, Naylor P, Mizel S B
Department of Microbiology and Immunology, Wake Forest University Medical Center, Winston-Salem, NC 27103.
J Immunol. 1989 Jun 15;142(12):4301-6.
Human Il-1 alpha induces the synthesis of kappa Ig L chains by the pre-B cell line 7OZ/3, IL-2R alpha by the human NK cell line YT, and PGE2 by human rheumatoid synovial cells. Pertussis toxin (PT) markedly inhibited all three IL-1-induced activation events. The inhibition by PT was associated with a decrease in IL-1-mediated cAMP production. PT also inhibited IL-1-stimulated cAMP production in crude membrane fractions from 7OZ/3, YT, and 3T3 fibroblasts. In addition, IL-1 stimulated GTPase activity present in the membranes IL-1-responsive cells. Furthermore, the IL-1-induced GTPase activity was sensitive to PT. PT induced the ADP-ribosylation of a 46-kDa substrate in membrane preparations from IL-1-responsive cells. Cholera toxin also induced the ADP-ribosylation of a 46-kDa substrate in the same membrane preparations. The present findings indicate that the IL-1R is linked to a PT-sensitive G protein that stimulates the activity of adenylate cyclase.
人白细胞介素-1α可诱导前B细胞系7OZ/3合成κ链免疫球蛋白轻链，诱导人自然杀伤细胞系YT合成白细胞介素-2受体α链，并诱导人风湿性滑膜细胞合成前列腺素E2。百日咳毒素（PT）显著抑制所有这三种白细胞介素-1诱导的激活事件。PT的抑制作用与白细胞介素-1介导的环磷酸腺苷（cAMP）生成减少有关。PT还抑制来自7OZ/3、YT和3T3成纤维细胞的粗膜组分中白细胞介素-1刺激的cAMP生成。此外，白细胞介素-1刺激白细胞介素-1反应性细胞膜中的GTP酶活性。而且，白细胞介素-1诱导的GTP酶活性对PT敏感。PT诱导白细胞介素-1反应性细胞膜制剂中一种46 kDa底物的ADP核糖基化。霍乱毒素也诱导相同膜制剂中一种46 kDa底物的ADP核糖基化。目前的研究结果表明，白细胞介素-1受体与一种对PT敏感的G蛋白相连接，该G蛋白可刺激腺苷酸环化酶的活性。
