Sussman G, Wadee A A
Department of Immunology, School of Pathology, University of the Witwatersrand, Johannesburg, Republic of South Africa.
Infect Immun. 1991 Aug;59(8):2828-35. doi: 10.1128/iai.59.8.2828-2835.1991.
The lipid component present in high-molecular-mass fractions with molecular masses of greater than 200 kDa derived from Mycobacterium tuberculosis extracts passaged through Sephacryl S.200 columns activate CD8+ lymphocytes to suppress lymphocyte blastogenesis. Suppression is mediated by the release of suppressor molecules by these CD8+ lymphocytes. Release of suppressor molecules occurs as early as 2 h following pulsing with the high-molecular-mass mycobacterial components and is maximal at 24 h, after which their release declines rapidly. Analysis by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western immunoblotting indicates that the active components are carbohydrate moieties with approximate molecular masses of 122 to 148 kDa. Our results suggest a mechanism of interaction between mycobacteria and host mononuclear cells such that mycobacterial lipids, once exposed, activate CD8+ suppressor lymphocytes. Activation of these lymphocytes results in the release of carbohydrate-containing molecules that ultimately inhibit the blastogenesis of other lymphocytes.
源自结核分枝杆菌提取物、分子量大于200 kDa的高分子量组分中存在的脂质成分，经Sephacryl S.200柱纯化后，可激活CD8+淋巴细胞，抑制淋巴细胞增殖。这种抑制作用是由这些CD8+淋巴细胞释放抑制分子介导的。在用高分子量分枝杆菌成分刺激后2小时，抑制分子就开始释放，24小时时释放量达到最大，之后其释放迅速下降。十二烷基硫酸钠-聚丙烯酰胺凝胶电泳和Western免疫印迹分析表明，活性成分是分子量约为122至148 kDa的碳水化合物部分。我们的结果提示了分枝杆菌与宿主单核细胞之间的一种相互作用机制，即分枝杆菌脂质一旦暴露，就会激活CD8+抑制性淋巴细胞。这些淋巴细胞的激活导致含碳水化合物分子的释放，最终抑制其他淋巴细胞的增殖。
