主体衍生的氧化脂在与微生物接触时启动效应器触发的免疫,促进致命性
Marco Di Gioia1, Valentina Poli1, Piao J Tan2
1Harvard Medical School and Boston Children's Hospital, Division of Immunology and Division of Gastroenterology, MA 02115, USA.
bioRxiv : the preprint server for biology
|December 4, 2023
概括
宿主衍生氧化脂 (oxPLs) 在微生物接触时出现,引发过度的炎症. 阻断oxPLs通过抑制AKT信号来保护宿主,为抗炎症疾病提供了一种新的治疗策略.
科学领域:
- 免疫学 免疫学 免疫学
- 分子生物学分子生物学
- 代谢过程中的代谢.
背景情况:
- 巨细胞利用模式识别受体和效应器触发免疫 (ETI) 来检测病原体.
- 感染造成的组织损伤释放出由宿主衍生的因素,加剧炎症.
- 这些自我衍生分子的感知机制和免疫影响尚未得到充分理解.
结论:
- 宿主衍生的炎症线索可以作为"自我"毒性因素,启动ETI.
- 准oxPL活动是一种潜在的治疗方法,可以缓解感染期间的过度炎症.
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