Chensue S W, Boros D L, David C S
J Exp Med. 1980 Jun 1;151(6):1398-412. doi: 10.1084/jem.151.6.1398.
Host granulomatous inflammation in murine schistosomiasis mansoni is a T cell-mediated immune response, which, at the chronic stage of the disease, undergoes T suppressor lymphocyte-dependent modulation. In the present study this phenomenon was further analyzed in vitro. Spleen cells of mice undergoing modulation (20 wk of infection) when mixed with spleen cells of animals exhibiting vigorous granulomatous responses (8 wk of infection) abrogated in vitro migration inhibition factor (MIF) production by the latter. Characterization of the delayed-type hypersensitivity T lymphocytes involved in lymphokine production showed that they belonged to the Lyt-1+ subset and did not express I region-encoded antigens. In contrast, T lymphocytes involved in the suppression of MIF activity belonged to the Lyt-2+ subpopulation of cells, which expressed I-J- and I-C-subregion determinants. These results suggest that the modulation of the granulomatous hypersensitivity response in mice is the result of T-T cell interaction with subsequent regulation of inflammatory lymphokine production.
宿主对曼氏血吸虫病的肉芽肿性炎症是一种T细胞介导的免疫反应,在疾病的慢性阶段,这种反应会受到T抑制淋巴细胞依赖性调节。在本研究中,对这一现象进行了进一步的体外分析。处于调节阶段(感染20周)的小鼠脾细胞与表现出强烈肉芽肿反应的动物(感染8周)的脾细胞混合时,会消除后者体外迁移抑制因子(MIF)的产生。对参与淋巴因子产生的迟发型超敏T淋巴细胞的特性分析表明,它们属于Lyt-1+亚群,不表达I区编码的抗原。相反,参与抑制MIF活性的T淋巴细胞属于Lyt-2+细胞亚群,该亚群表达I-J和I-C亚区决定簇。这些结果表明,小鼠肉芽肿性超敏反应的调节是T-T细胞相互作用以及随后对炎性淋巴因子产生进行调节的结果。