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氨基酸及其转运体对树突状细胞生物学的调控。

Regulation of dendritic cell biology by amino acids and their transporters.

作者信息

Chen Shanlin, Li Gongwei, Jiang Zihao, Xu Yuekang, Aipire Adila, Li Jinyao

机构信息

Xinjiang Key Laboratory of Biological Resources and Genetic Engineering, College of Life Science & Technology, Xinjiang University, Urumqi, China.

出版信息

Front Immunol. 2025 Jul 4;16:1626973. doi: 10.3389/fimmu.2025.1626973. eCollection 2025.

Abstract

Dendritic cells (DCs) play a central role in inducing both immunity and tolerance as specialized antigen-presenting cells (APCs). The immunometabolic firestorm in recent years has focused our attention on how DCs use energy and respond to nutritional changes that affect immune functions. Like in every other cell, such metabolic events as the concentration of free amino acids, membrane-bound transporter proteins, key metabolic enzymes, and sensors (e.g., mTOR and GCN2), also profoundly affect the function and fate of DCs. Therefore, dysregulation of amino acid metabolism can cause metabolic reprogramming of DCs, leading to or accelerating the occurrence of various immunological disorders, like type 1 diabetes, rheumatoid arthritis, and cancer. Since amino acids cannot directly enter the cell to participate in metabolic activities, their transporters act as critical metabolic gatekeepers. To catch up with the rapid development in the immune metabolism field, this review summarized recent studies on the potential roles of different amino acids and their transporters in the regulation of DCs biology to offer new insights for immune-dysregulated diseases and explore new therapeutic targets.

摘要

树突状细胞(DCs)作为特殊的抗原呈递细胞(APCs),在诱导免疫和耐受方面发挥着核心作用。近年来的免疫代谢热潮使我们关注DCs如何利用能量以及对影响免疫功能的营养变化做出反应。与其他细胞一样,诸如游离氨基酸浓度、膜结合转运蛋白、关键代谢酶和传感器(如mTOR和GCN2)等代谢事件,也深刻影响着DCs的功能和命运。因此,氨基酸代谢失调可导致DCs的代谢重编程,从而引发或加速各种免疫紊乱的发生,如1型糖尿病、类风湿性关节炎和癌症。由于氨基酸不能直接进入细胞参与代谢活动,它们的转运蛋白充当着关键的代谢守门人。为跟上免疫代谢领域的快速发展,本综述总结了近期关于不同氨基酸及其转运蛋白在调节DCs生物学方面潜在作用的研究,为免疫失调疾病提供新见解,并探索新的治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0bf2/12271228/97b958e669c4/fimmu-16-1626973-g001.jpg

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