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CD8+ T细胞的免疫代谢缺陷破坏了艾滋病毒感染者的肠道屏障完整性

Upasana Das Adhikari¹, Leah M Froehle¹, Alexandra N Pipkin¹

¹Ragon Institute of Mass General Brigham, MIT and Harvard, Cambridge, MA 02139, USA.

|September 12, 2025

概括

艾滋病毒通过CD8+T细胞的免疫代谢缺陷破坏了肠道屏障的完整性. 这些细胞会损害脂质代谢,导致上皮细胞死亡和肠道平衡的丧失.

科学领域:

免疫学
胃肠病学
代谢过程

背景情况:

即使在抗逆转录病毒治疗 (ART) 中,肠道屏障的破坏也是艾滋病毒感染的持续特征.
导致艾滋病毒感染者的持续性肠损伤的确切机制尚未完全理解.
这种受损的屏障功能与艾滋病毒疾病的进展有关.

研究的目的:

阐明肠内CD8+T细胞对PWH肠道屏障功能障碍的免疫代谢机制.
确定与HIV相关的T细胞代谢如何影响肠道上皮细胞.

主要方法:

来自艾滋病毒感染者 (PWH) 和对照者的结肠 CD8+ T 细胞的分析.
评估过氧体增殖器激活受体-γ (PPARγ) 表达和脂质代谢.
评估脂肪滴积累和脂肪酸氧化情况.
研究CD8+T细胞和肠上皮细胞之间的相互作用.

主要成果:

在PWH中的结肠CD8+T细胞呈现下调的过氧体增殖器激活受体-γ (PPARγ).
这种下调导致细胞内脂质滴的减少和T细胞中的脂肪酸氧化受损.
感染HIV的T细胞从肠道上皮细胞中获取脂质,从而促进上皮细胞的亡.
这种过程会破坏肠上皮质平衡.

结论:

结肠CD8+T细胞的与HIV相关的免疫代谢失调是肠道屏障破坏的关键驱动因素.
缺陷的PPARγ信号和T细胞改变的脂质处理有助于上皮细胞死亡.
针对这些免疫代谢途径可以提供恢复肠道完整性和减少PWH的并发症的策略.

关键词:

艾滋病毒肠道屏障的完整性免疫-上皮相互作用免疫新陈代谢肠上皮细胞组织中存在的CD8+T细胞

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