Evidence map›Paper›PMID 41927788›Full record

ArticleCellular & molecular immunology2026

Acute stress alleviates type 2 lung inflammation by restricting ILC2s through corticosterone-glucocorticoid receptor signaling.

Lin Zhu, Yuying Huang, Bo Peng, Shufeng Zhong, Xiaoyu Zhang, Fuyang Xiao, Dilare Asim, Jieken Pakezhati, Jinquan Ma, Siying Sun and 8 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. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

18 authors.

Lin Zhu *Key Laboratory of Multi-Cell Systems, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Yuying Huang *Key Laboratory of Multi-Cell Systems, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.ORCID 0009-0001-1107-2646
Bo Peng *Department of Pulmonary and Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0001-5697-7396
Shufeng ZhongKey Laboratory of Multi-Cell Systems, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.ORCID 0009-0007-5307-8572
Xiaoyu ZhangDepartment of Allergy, People's Hospital of Xinjiang Uygur Autonomous Region, Xinjiang Urumqi, China.
Fuyang XiaoDepartment of Allergy, People's Hospital of Xinjiang Uygur Autonomous Region, Xinjiang Urumqi, China.
Dilare AsimGraduate school of Xinjiang Medical University, Urumqi, China.
Jieken PakezhatiGraduate school of Xinjiang Medical University, Urumqi, China.
Jinquan MaGraduate school of Xinjiang Medical University, Urumqi, China.
Siying SunDepartment of Pulmonary and Critical Care Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Jiefang XuSchool of Life Science, University of Science and Technology of China, Hefei, China.
Shipeng ChengKey Laboratory of Multi-Cell Systems, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Liyan MaKey Laboratory of Multi-Cell Systems, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Zhiyang LingKey Laboratory of Multi-Cell Systems, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.ORCID 0000-0001-8873-6773
Chuyan YiKey Laboratory of Multi-Cell Systems, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Dongmei LuCenter for Pulmonary and Critical Care Medicine, Peoples Hospital of Xinjiang Uygur Autonomous Region, Xinjiang Urumqi, China. dongmeilu2009@sina.com.
Junqin LiangDepartment of Allergy, People's Hospital of Xinjiang Uygur Autonomous Region, Xinjiang Urumqi, China. drliangjq@163.com.
Bing SunKey Laboratory of Multi-Cell Systems, Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China. bsun@sibs.ac.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The psychological state profoundly influences immune responses. While chronic stress is generally known to exacerbate inflammation, the impact of acute stress on inflammation has received far less attention. Here, we report that acute stress suppressed group 2 innate lymphoid cell (ILC2) responses, thereby alleviating type 2 lung inflammation. Restraint stress-induced acute stress activated the hypothalamic-pituitary-adrenal (HPA) axis and subsequently increased corticosterone levels. Corticosterone protected mice against lung inflammation by limiting ILC2 proliferation and type 2 cytokine production via the glucocorticoid receptor (GR). Adrenalectomy and genetic perturbation of the GR in ILC2s abolished acute stress-mediated immunosuppressive effects. Mechanistic studies revealed that corticosterone-GR signaling impaired ILC2 responses to microenvironmental factors by dampening downstream NF-κB and JAK-STAT signaling. Collectively, these findings reveal that acute stress alleviates ILC2-mediated lung inflammation through the neuroendocrine circuit and demonstrate the inhibitory role of endogenous corticosterone in ILC2 responses.

Indexed as

CorticosteroneImmunity, InnateLymphocytesPneumoniaReceptors, GlucocorticoidSignal TransductionStress, PhysiologicalAnimalsCytokinesHypothalamo-Hypophyseal SystemMaleMiceMice, Inbred C57BLPituitary-Adrenal SystemCorticosteroneCytokinesReceptors, GlucocorticoidAcute stressCorticosteroneGlucocorticoid receptorGroup 2 innate lymphoid cellHPA axisLung inflammation

Identifiers

PMID41927788
PMCPMC13128937

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.