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介酶体 stromal 细胞通过淋巴结内的 L-氨基酸氧化酶抑制 Th17 细胞反应

Qi Ni¹, Le Zhen¹, Zhu Zeng¹

¹Key Laboratory of Drug Metabolism and Pharmacokinetics, Haihe Laboratory of Cell Ecosystem, State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing, China.

Cell death & disease

|September 9, 2024

概括

在自身免疫性疾病模型中,中酶体 stromal 细胞 (MSC) 向淋巴结,通过 L-氨基酸氧化酶 (LAAO) 和英-3-酸 (I3P) 抑制炎症 Th17 细胞,以获得治疗效益.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
治疗方法治疗方法

背景情况:

介酶体 stromal/干细胞 (MSC) 在自身免疫性疾病中显示出治疗潜力.
了解MSC免疫调节机制对于优化治疗至关重要.

研究的目的:

在自身免疫性疾病模型中阐明人类带MSC的指导机制和免疫调节功能.
确定参与MSC介导的Th17细胞抑制的关键分子通路.

主要方法:

在自身免疫疾病小鼠模型的淋巴结中跟踪人类带MSC.
分析CCL21-CCR7轴表达及其在MSC定位中的作用.
通过MSC对Th17细胞调节的评估及其对L-氨基酸氧化酶 (LAAO) 和-3-酸 (I3P) 的依赖.
研究TNF-α,NF-κB和AHR通路的参与.

主要成果:

人类带MSC选择性聚合在自身免疫性疾病小鼠的淋巴结中,而不是健康的对照,由于CCL21-CCR7轴的上调.
通过TNF-α/NF-κB通路,MSC诱导了L-氨基酸氧化酶 (LAAO) 的分泌,这对于抑制Th17细胞至关重要.
由LAAO衍生而来的-3-酸 (I3P) 通过激活基碳水化合物受体 (AHR) 途径来抑制Th17细胞.

结论:

在自身免疫性疾病中,MSC指向淋巴结的指导由CCL21-CCR7轴介导.
通过分泌LAAO,MSC通过产生I3P来通过AHR途径抑制Th17细胞,从而产生抗炎作用.
这些发现为基于MSC的自身免疫疾病免疫调节提供了洞察力.

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