文献类型：期刊文献

英文题名：Type 2 Inflammatory Diseases: The Crossroads of Immunity and Metabolism

作者：Chen, Lin[1,2];Pan, Zhou-Xian[1];Ma, Zi-Qi[3];Jin, Yu-Xuan[1];Ru, Yi[1];Gao, Pei-Song[4];Yang, Cheng[1];Zhao, Shi-Su[1];Zhang, Jing[1];Li, Ji-Han[1];Chang, Christopher[5];Zhao, Yu-Zheng[2];Sun, Jin-Lyu[1]

机构：[1]Chinese Acad Med Sci & Peking Union Med Coll, Peking Union Med Coll Hosp, Dept Allergy, State Key Lab Complex Severe & Rare Dis, Beijing 100730, Peoples R China;[2]East China Univ Sci & Technol, Optogenet & Synthet Biol Interdisciplinary Res Ctr, Shanghai Frontiers Sci Ctr Optogenet Tech Cell Met, State Key Lab Bioreactor Engn,Sch Pharm, Shanghai 200237, Peoples R China;[3]Chinese Acad Med Sci, Peking Union Med Coll,Dept Biochem & Mol Biol, Dept Mol Biol & Biochem,Inst Basic Med Sci, Sch Basic Med,Neurosci Ctr,Med Primate Res Ctr, Beijing 100005, Peoples R China;[4]Johns Hopkins Univ, Sch Med, Div Allergy & Clin Immunol, Baltimore, MD 21224 USA;[5]Joe DiMaggio Childrens Hosp, Div Immunol Allergy & Pediat Rheumatol, Mem Healthcare Syst, Hollywood, FL 33021 USA

年份：2026

卷号：9

外文期刊名：RESEARCH

收录：;EI(收录号：20262821089096);Scopus(收录号：2-s2.0-105044281252);WOS:【SCI-EXPANDED(收录号:WOS:001813482100001)】；

基金：This study was financially supported by the National High-Level Hospital Clinical Research Funding (2022-PUMCH-D-002), the Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences (2021-I2M-1-017), and the Peking Union Medical College Hospital Talent Cultivation Program Category D (UHB12266).

语种：英文

外文关键词：Diagnosis - Diseases - Metabolism - Pathology - Physiology - Signaling - Thorium compounds - Tissue - Tissue homeostasis

摘要：The understanding of type 2 inflammatory diseases is undergoing a paradigm shift from "immune imbalance" toward "immune-metabolic crosstalk". Energy metabolism not only fuels immune responses but also fundamentally dictates the functional phenotypes of immune cells through metabolic reprogramming. By systematically integrating metabolic programming data of key immune cells across diverse tissues (skin, gut, nasal, and ocular mucosa), this review constructs a cross-disease "metabolism-signaling network" atlas. The synthesis highlights that glycolysis and mTORC1 signaling are predominantly coupled with the pro-inflammatory outputs of Th2 cells and ILC2s, whereas fatty acid oxidation (FAO) and oxidative phosphorylation (OXPHOS) sustain the homeostasis of Tregs and M2-like macrophages. Furthermore, this review characterizes how the tryptophan, glutamine, and arginine pathways fine-tune the immune tolerance boundary via the IDO-AhR-mTOR axis. We also elucidate a conserved inter-organ "hypoxia-HIF-1 alpha-lactylation" axis, which, in conjunction with tissue-specific metabolic branches (e.g., the ceramide pathway in the skin, the SCFA circuit in the gut, and the lactate-GPR81 loop in the mucosa), collectively sculpts local microenvironments and remodeling trajectories. Ultimately, a novel diagnostic and therapeutic framework centered on metabolic phenotyping is proposed, providing prospective insights into targeting metabolic checkpoints for precision immunotherapy in type 2 inflammation.