Evidence map›Paper›PMID 41593294›Full record

ArticleCellular & molecular immunology2026

Obesity disrupts ILC2 metabolic and functional homeostasis by inhibiting mTORC1 signaling.

Lin Hu, Dongdi Wang, Yue Chen, Jinxin Qiu, Hongdong Wang, Youqin Zhang, Michelle Zhang, Xiaohui Su, Ju Qiu, Jiping Sun and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular & molecular immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Metabolic Reprogramming and ILC2 Plasticity in Obesity-related Asthma.Clinical reviews in allergy & immunology · 2026
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Lin Hu *Center for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Dongdi Wang *Center for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yue ChenCAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Jinxin QiuCAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.
Hongdong WangDepartment of Endocrinology, Drum Tower Hospital affiliated with Nanjing University Medical School, Branch of National Clinical Research Centre for Metabolic Diseases, Nanjing, China.
Youqin ZhangCenter for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Michelle ZhangDepartment of Immunology and Microbiology, Key Laboratory of Cell Differentiation and Apoptosis of Chinese Ministry of Education, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xiaohui SuCenter for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Ju QiuCAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.ORCID 0000-0002-1543-5678
Jiping SunCenter for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. sunjiping@shsmu.edu.cn.
Lei ShenCenter for Immune-Related Diseases at Shanghai Institute of Immunology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China. lshen@shsmu.edu.cn.ORCID 0000-0003-2811-7094

Funding

Ministry of Science and Technology of the People's Republic of China (Chinese Ministry of Science and Technology) grant 2020YFA0509200National Natural Science Foundation of China (National Science Foundation of China) grants 32250710147 and 81971487Science and Technology Commission of Shanghai Municipality (Shanghai Municipal Science and Technology Commission) grant 23ZR1455100
6 · The paper itself

Abstract

Group 2 innate lymphoid cells (ILC2s) play crucial roles in maintaining adipose tissue homeostasis. Recent studies indicate that ILC2s are dysregulated in obesity. However, the regulatory mechanisms governing adipose tissue ILC2 function remain inadequately explored. In this study, we demonstrated that mechanistic target of rapamycin complex 1 (mTORC1) activity is impaired in adipose tissue ILC2s from obese mice and humans. Deletion of Raptor, a critical adaptor protein in mTORC1, results in reduced numbers of ILC2s and diminished type 2 cytokine production in ILC2s, leading to increased adipose tissue inflammation and insulin resistance. Mechanistically, mTORC1 signaling upregulates PPARγ expression through HIF-1α, which promotes mitochondrial biogenesis and ST2 expression to sustain ILC2 metabolic and functional fitness. Together, our data identify mTORC1 as a crucial regulator that coordinates adipose tissue ILC2 metabolic and immunological homeostasis and prevents obesity-associated insulin resistance.

Indexed as

HomeostasisImmunity, InnateLymphocytesMechanistic Target of Rapamycin Complex 1ObesitySignal TransductionAdipose TissueAnimalsCytokinesHumansHypoxia-Inducible Factor 1, alpha SubunitInsulin ResistanceMiceMice, Inbred C57BLPPAR gammaRegulatory-Associated Protein of mTORCytokinesHypoxia-Inducible Factor 1, alpha SubunitMechanistic Target of Rapamycin Complex 1PPAR gammaRegulatory-Associated Protein of mTORGroup 2 innate lymphoid cellsmTORC1PPARγST2

Identifiers

PMID41593294
PMCPMC12948970

What OpenQuestion holds

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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.