Evidence map›Paper›PMID 42340414›Full record

ArticleJournal of gastroenterology2026

Mucosal-associated invariant T cells promote PDAC progression via TL1A-CSF-1 axis.

Longyun Ye, Qinglin Fei, Tianjiao Li, Huiyi Ou, Shuai Wang, Yiting Zhang, Yi Zhou, Xianjun Yu, Kaizhou Jin, Weiding Wu

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Article in Journal of gastroenterology, 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

What it found

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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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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

10 authors.

Longyun Ye *Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Qinglin Fei *Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Tianjiao Li *Department of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Huiyi OuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Shuai WangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Yiting ZhangDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Yi ZhouDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.
Xianjun YuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. yuxianjun@fudanpci.org.
Kaizhou JinDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. jinkaizhou@fudanpci.org.
Weiding WuDepartment of Pancreatic Surgery, Fudan University Shanghai Cancer Center, Shanghai, 200032, China. wuweiding@fudanpci.org.ORCID http://orcid.org/0000-0002-7188-1066

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMucosal-associated invariant T (MAIT) cells have been implicated in several malignancies, but their role in pancreatic ductal adenocarcinoma (PDAC) remains unclear. This study aimed to characterize the presence, phenotype, and functional role of MAIT cells in PDAC and explore the underlying regulatory mechanisms.

methodsWe analyzed human PDAC tissue samples using single-cell RNA sequencing and flow cytometry to evaluate MAIT cell abundance and phenotype. Functional studies were performed in MR1-deficient (Mr1

resultsMAIT cells were significantly enriched in PDAC tissues and associated with poor patient survival. Further studies inMR1-deficient (Mr1

conclusionsOur findings reveal a novel TL1A-MAIT-CSF-1 axis that drives immunosuppression in PDAC by reprogramming innate immune responses. Targeting MAIT cells or TL1A signaling may represent a promising therapeutic strategy to improve immunotherapy efficacy in PDAC.

Indexed as

CSF-1Mucosal-associated invariant T (MAIT)PDACTL1A

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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.