Turco J, Winkler H H
Infect Immun. 1983 Oct;42(1):27-32. doi: 10.1128/iai.42.1.27-32.1983.
Certain properties of the antirickettsial activity and interferon in lymphokine preparations obtained from concanavalin A-stimulated mouse spleen cells were compared. Both the antirickettsial activity and interferon were relatively stable to heating at 56 degrees C, whereas both activities were destroyed by trypsin, by heating at 80 degrees C, or by exposure to pH 2 for 24 h. Both activities were likewise inhibited after incubation with rabbit antisera to partially purified murine interferon-gamma. In contrast to the mouse lymphokine preparations, which contained both interferon-gamma and antirickettsial activity, a preparation of virus-induced interferons (type I) had no detectable antirickettsial activity. Human foreskin fibroblasts, which were not sensitive to the antirickettsial activity in mouse lymphokines, acquired the ability to inhibit rickettsial growth when they were cocultured with sensitive mouse L929 cells treated with mouse lymphokines. These results are consistent with the idea that the antirickettsial activity in mouse lymphokines is due to interferon-gamma.
对从伴刀豆球蛋白A刺激的小鼠脾细胞中获得的淋巴因子制剂中的抗立克次体活性和干扰素的某些特性进行了比较。抗立克次体活性和干扰素在56℃加热时相对稳定,而两种活性均可被胰蛋白酶、80℃加热或暴露于pH 2环境24小时所破坏。在用兔抗部分纯化的小鼠γ干扰素血清孵育后,两种活性同样受到抑制。与含有γ干扰素和抗立克次体活性的小鼠淋巴因子制剂不同,病毒诱导的I型干扰素制剂没有可检测到的抗立克次体活性。对小鼠淋巴因子中的抗立克次体活性不敏感的人包皮成纤维细胞,当与用小鼠淋巴因子处理过的敏感小鼠L929细胞共培养时,获得了抑制立克次体生长的能力。这些结果与小鼠淋巴因子中的抗立克次体活性归因于γ干扰素的观点一致。