CD8在T. brucei brucei释放的分子的淋巴细胞激活中具有关键作用
T Olsson1, M Bakhiet, B Höjeberg
1Department of Neurology, Karolinska Institute, Huddinge Hospital, Sweden.
Cell
|March 12, 1993
概括
非洲试杆菌寄生虫释放了一种激活CD8+T细胞产生IFN-的因子,促进寄生虫的生长. 阻止这种相互作用可以提高宿主生存率.
科学领域:
- 免疫学 免疫学 免疫学
- 寄生虫学的寄生虫学
- 分子生物学分子生物学
背景情况:
- 由T. brucei brucei引起的非洲虫病是一种重要的寄生虫疾病.
- 宿主对T. brucei brucei感染的免疫反应涉及寄生虫因素和宿主细胞之间的复杂相互作用.
研究的目的:
- 研究T. brucei brucei影响宿主T细胞反应的机制.
- 识别调节T细胞激活和细胞因子生产的寄生虫衍生因素.
主要方法:
- 从T. brucei brucei中净化和表征淋巴细胞触发因子 (TLTF).
- 在实验室测试使用纯化的CD8+和CD4+T细胞,单核细胞 (MNC) 培养物和T. brucei brucei感染的小鼠.
- 对细胞因子mRNA表达的分析 (IFN-玛,TGF-β,IL-4) 和 [3H] 提米丁的结合.
- 使用抗CD8抗体和可溶性CD8的阻断实验.
- 对来自CD8缺乏突变小鼠的T细胞的研究.
主要成果:
- TLTF 特别触发了 CD8+ T 细胞,诱导干扰素玛 (IFN-玛) mRNA 表达,分泌和 [3H] 提米丁的结合.
- 此外,TLTF还诱导了转化生长因子β mRNA,但并没有诱导介素-4.
- TLTF的作用被抗CD8抗体和可溶性CD8阻断,并且在CD8缺乏细胞中不存在.
- IFN-玛作为T. brucei. brucei的生长刺激剂.
- 与CD8+小鼠相比,缺乏CD8表达 (CD8-) 的小鼠表现出较低的寄生素血症和延长的存活时间.
结论:
- 在非洲试验性试虫病中的宿主-寄生虫相互作用涉及寄生虫释放的TLTF.
- TLTF与CD8结合,激活CD8+ T细胞产生IFN-,一种促进寄生虫生长的细胞因子.
- 针对这种CD8介导的免疫反应可能是治疗非洲试索米亚症的治疗策略.
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