来自克罗恩病微生物群的溶血磷脂酰丝氨酸引起病理性Th1反应

Yuriko Otake-Kasamoto, H. Kayama, T. Kishikawa, S. Shinzaki, T. Tashiro, Takahiro Amano, M. Tani, T. Yoshihara, Bo Li, Haruka Tani, Li Liu, Akio Hayashi, D. Okuzaki, D. Motooka, S. Nakamura, Y. Okada, H. Iijima, K. Takeda, T. Takehara
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引用次数: 8

摘要

这项研究表明,克罗恩病相关的微生物群产生溶血磷脂酰丝氨酸,通过促进糖酵解促进Th1反应。CD4+ T细胞缺乏P2y10可预防溶血磷脂酰丝氨酸引起的结肠炎加重,这表明益生菌来源的溶血磷脂酰丝氨酸通过调节Th1细胞代谢加剧结肠炎。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Lysophosphatidylserines derived from microbiota in Crohn’s disease elicit pathological Th1 response
This study shows that Crohn’s disease–associated microbiota generate lysophosphatidylserines that promote Th1 responses by fueling glycolysis. Lysophosphatidylserine-induced aggravation of colitis is prevented by P2y10 deficiency in CD4+ T cells, demonstrating that dysbiotic microbiota-derived LysoPS exacerbates colitis by modulating Th1 cell metabolism.
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