在慢性寄生虫感染期间,CD4+ T细胞调节疾病诱导的厌食症和脂肪消耗
Samuel E Redford1, Siva Karthik Varanasi2, Karina K Sanchez3
1Molecular and Systems Physiology Lab, Salk Institute for Biological Studies, 10010 N. Torrey Pines Road, La Jolla, CA 92037, USA; Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92037, USA; NOMIS Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studies, La Jolla, CA, USA; Gene Expression Lab, Salk Institute for Biological Studies, 10010 N. Torrey Pines Road, La Jolla, CA 92037, USA.
适应性免疫力驱动着与感染相关的消耗. CD4+ T 细胞导致脂肪损失,而 CD8+ T 细胞在两相反应中诱导肌肉消耗 (缓解症).
科学领域:
- 免疫学 免疫学 免疫学
- 寄生虫学的寄生虫学
- 代谢过程中的代谢.
背景情况:
- 感染会引发体质丧失,影响脂肪和肌肉储存.
- 天生的免疫系统在消耗中的作用是已知的,但适应性免疫系统的贡献是不清楚的.
- 了解适应性免疫在感染引起的衰竭中的作用,对于疾病管理至关重要.
研究的目的:
- 调查适应性免疫系统在感染期间脂肪组织消耗和缓解症中的作用.
- 阐明涉及不同阶段消耗的特异性T细胞子集.
- 为了确定免疫介导抵抗和代谢反应之间的关系.
主要方法:
- 使用慢性寄生虫感染 (Trypanosoma brucei) 的小鼠模型.
- 分析了CD4+和CD8+T细胞在浪费过程中的不同作用.
- 评估脂肪浪费对宿主防御和生存的影响.
主要成果:
- 消耗反应分为两个阶段进行:CD4+ T细胞介导的厌食症导致脂肪消耗,其次是CD8+ T细胞依赖的缓解症.
- 脂肪消耗不会阻碍抗体介导的耐药性或生存.
- 晚期肌肉消耗有助于疾病耐受性.
结论:
- 适应性免疫在感染诱导的代谢中起着关键的,分阶段的作用.
- 在适应性免疫介导抵抗和感染期间身体的代谢反应之间存在分离.
- 这项研究突出了T细胞在调解抵抗与代谢中断方面的独特功能.
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