Evidence map›Paper›PMID 41896941›Full record

ArticleCell communication and signaling : CCS2026

ILC2-derived IL-9 activates regulatory T cells to facilitate post-myocardial infarction repair.

Yuxiao Feng, Rongjiao Shao, Yiping Shi, Haibei Sun, Chen Chi, Weizhuo Liu, Bin He, Wenzheng Han, Xumin Hou

Abstract read
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In one paragraph

Article in Cell communication and signaling : CCS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Yuxiao Feng *Department of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.ORCID http://orcid.org/0009-0000-4914-138X
Rongjiao Shao *Department of Critical Care Medicine and Emergency, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.ORCID http://orcid.org/0000-0002-1082-560X
Yiping Shi *Department of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Haibei SunDepartment of Critical Care Medicine and Emergency, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Chen ChiDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Weizhuo LiuDepartment of Critical Care Medicine and Emergency, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Bin HeDepartment of Critical Care Medicine and Emergency, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China. bin_he@sjtu.edu.cn.ORCID http://orcid.org/0000-0001-8468-7492
Wenzheng HanDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China. wzhan_cardiology@foxmail.com.
Xumin HouDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China. houxumin@sjtu.edu.cn.ORCID http://orcid.org/0000-0002-0505-7642

Funding

Key Discipline of Shanghai Municipal Health System 2023ZDFC0105National Natural Science Foundation of China 82172168, 82372202National Natural Science Foundation of China 82302458National Natural Science Foundation of China 82400509National Natural Science Foundation of China 82472216,82272228Program of Shanghai Academic/Technology Research Leader 23XD1403500Shanghai Sailing Program from the Shanghai Science and Technology Committee 23YF1432800
6 · The paper itself

Abstract

backgroundGroup 2 innate lymphoid cells (ILC2s) are recognized as key innate immune effectors that facilitate early cardiac recovery after myocardial infarction (MI); however, the underlying mechanisms by which they mediate this repair remain largely unclear.

methodsTo investigate the role of ILC2-derived interleukin-9 (IL-9), we employed ILC2-specific IL-9 knockout mice and administered exogenous IL-9 in a murine MI model. The mechanism of regulatory T cells (Tregs) activation was further examined through Treg-specific Sirt1 knockout in vitro, focusing on STAT5 acetylation and related signaling.

resultsWe demonstrate that ILC2-derived IL-9 is essential for post-MI repair by activating Tregs. IL-9 binding to the IL-9 receptor on Tregs upregulates the deacetylase Sirt1, and Sirt1 deletion abolishes IL-9-driven Treg activation. Furthermore, Sirt1 directly interacts with STAT5, promoting its deacetylation and phosphorylation, leading to the transcriptional activation of genes essential for Treg function.

conclusionOur study identifies IL-9 as a key regulator of Treg activation via a novel Sirt1-STAT5 epigenetic pathway, which promotes tissue repair after MI. These findings reveal a previously unrecognized immunomodulatory axis with significant therapeutic potential for ischemic heart disease.

Indexed as

Immunity, InnateInterleukin-9Lymphocyte ActivationLymphocytesMyocardial InfarctionT-Lymphocytes, RegulatoryAcetylationAnimalsMaleMiceMice, Inbred C57BLMice, KnockoutSignal TransductionSirtuin 1STAT5 Transcription FactorInterleukin-9Sirt1 protein, mouseSirtuin 1STAT5 Transcription FactorILC2Interleukin 9Myocardial infarctionRegulatory T cellsSirt1

Identifiers

PMID41896941
PMCPMC13147629

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.