Evidence map›Paper›PMID 41974707›Full record

ArticleNature communications2026

JAK inhibitors alleviate EGFR-inhibitor-induced diarrhea by protecting intestinal stem cells from adaptive-immune-exacerbated injury.

Yuan Cheng, Chenyue Xu, Dazhao Lv, Meng Tian, Haoyu Wang, Bingxue Yang, Leying Chen, Qing You, Shiyi Zhang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 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

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

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

9 authors.

Yuan ChengSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Chenyue XuSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Dazhao LvSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Meng TianSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.ORCID http://orcid.org/0000-0001-7719-9896
Haoyu WangSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Bingxue YangSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Leying ChenSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Qing YouSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China. youqing@sjtu.edu.cn.ORCID http://orcid.org/0000-0001-6455-2670
Shiyi ZhangSchool of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China. zhangshiyi@sjtu.edu.cn.ORCID http://orcid.org/0000-0002-9375-5992

Funding

National Natural Science Foundation of China (National Science Foundation of China) T2550061Shanghai Municipal Education Commission ZXWH1082101
6 · The paper itself

Abstract

While intestinal stem cells (ISC) are essential for epithelial homeostasis, their dynamic regulation during immune-mediated injury remains undefined. Here we show that suppression of jejunal ISC proliferation contributes to pathology arising from oral EGFR (epidermal growth factor receptor) tyrosine kinase inhibitor (TKI) treatment. Suppression of adaptive immunity via genetic intervention reverses ISC suppression and accelerates mucosal repair via inhibiting the TKI-induced, chemokine-directed migration of T and B lymphocytes from Peyer's patches. Spatial transcriptomics reveals enhanced crosstalk between adaptive immune cells and ISCs in the jejunum. Ex vivo modelling demonstrates that activated T cells directly impair ISC survival through IFN-γ and TNF, with IFN-γ-induced JAK (Janus kinase) /STAT signaling serving as a critical downstream effector. Accordingly, targeted JAK inhibition mitigates EGFRi (epidermal growth factor receptor inhibitor)-induced diarrhea without substantially compromising antitumor efficacy. This work thus redefines TKI-induced enteropathy as an immune-driven pathology and identifies JAK inhibition as a mechanism-based supportive management of targeted therapy toxicities.

Indexed as

Adaptive ImmunityDiarrheaJanus KinasesProtein Kinase InhibitorsStem CellsAnimalsB-LymphocytesCell ProliferationErbB ReceptorsFemaleInterferon-gammaIntestinal MucosaJejunumMaleMiceMice, Inbred C57BLEGFR protein, mouseErbB ReceptorsInterferon-gammaJanus KinasesProtein Kinase InhibitorsQuinazolines

Identifiers

PMID41974707
PMCPMC13249821

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.