Evidence map›Paper›PMID 41491580›Full record

ArticleEuropean journal of medical research2026

Proliferation, migration, and differentiation of circulating ILC precursors in HBV infection-associated fibrosis.

Qin Zhu, Fang-Yuan Chen, Shi-Qin Li, Cheng-Zhao Weng, Si-Qi Wang, Lin-Lin Zheng, Yong-Yu Yang, Li Xie, Jian Wu, Wei Jiang

Abstract read
In one paragraph

Article in European journal of medical research, 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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0citing papers 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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4 · The record

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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

10 authors.

Qin ZhuDepartment of Gastroenterology and Hepatology, Zhongshan Hospital (Xiamen), Fudan University, Xiamen, 361015, China.
Fang-Yuan ChenDepartment of Infectious Diseases, Zhongshan Hospital, Fudan University, Shanghai, 200032, China.
Shi-Qin LiDepartment of Gastroenterology and Hepatology, Zhongshan Hospital (Xiamen), Fudan University, Xiamen, 361015, China.
Cheng-Zhao WengDepartment of Gastroenterology and Hepatology, Zhongshan Hospital (Xiamen), Fudan University, Xiamen, 361015, China.
Si-Qi WangShanghai Institute of Infectious Disease and Biosecurity, Fudan University, Shanghai, 200032, China.
Lin-Lin ZhengDepartment of Gastroenterology and Hepatology, Zhongshan Hospital of Fudan University, 180 Fenglin Road, Shanghai, 200032, China.
Yong-Yu YangDepartment of Medical Microbiology and Parasitology, MOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University Shanghai Medical College, Shanghai, 200032, China.
Li XieDepartment of Medical Microbiology and Parasitology, MOE/NHC/CAMS Key Laboratory of Medical Molecular Virology, School of Basic Medical Sciences, Fudan University Shanghai Medical College, Shanghai, 200032, China.
Jian WuDepartment of Gastroenterology and Hepatology, Zhongshan Hospital of Fudan University, 180 Fenglin Road, Shanghai, 200032, China.
Wei JiangDepartment of Gastroenterology and Hepatology, Zhongshan Hospital (Xiamen), Fudan University, Xiamen, 361015, China. jiang.wei@zs-hospital.sh.cn.ORCID http://orcid.org/0000-0002-9354-6699

Funding

Fujian provincial medical innovation project (2022CXB020)Fujian Provincial Natural Science Foundation Project (2021D033)Natural science foundation of China (82200683)Natural science foundation of China (82370622)Natural science foundation of China (82370625, 82170624)Shanghai Sailing Program (22YF1445900)
6 · The paper itself

Abstract

backgroundIncreased studies indicate that innate lymphoid cells (ILCs) are involved in inflammatory and immune responses in chronic liver injury. However, recruitment and maturation of their subsets during hepatic fibrosis post-HBV infection are unknown. The present study aims to explore the potential impact of ILC precursors (ILCPs) on the modulation of HBV infection-associated fibrosis.

methodsPeripheral blood mononuclear cells (PBMCs) from healthy controls (HCs), chronic hepatitis B infected (CHB), and cirrhotic patients and lymphoid and splenic mononuclear cells from HBV-transgenic mice were isolated to determine the richness of ILC precursors (ILCPs) and ILC subsets by flow cytometry.

resultsThe richness of ILCPs and ILC3 subsets was significantly increased in PBMCs of patients with chronic hepatitis B infection and in lymph nodes and spleens of HBV-transgenic mice with carbon tetrachloride treatment. Importantly, among these ILCPs, the percentage of CD62L and CXCR6-expressing ILCPs were proportionally enriched. IL-23 may contribute to CD62L

conclusionThe microenvironment of HBV infection-associated fibrosis enhances the proliferation, migration, and differentiation of peripheral ILCPs and IIL-23, and Notch signaling pathways may play significant roles in these processes.

Indexed as

Hepatitis B, ChronicLiver CirrhosisLymphocytesAdultAnimalsCell DifferentiationCell MovementCell ProliferationFemaleHepatitis B virusHumansImmunity, InnateMaleMiceMice, TransgenicMiddle AgedChronic hepatitis B infectionCirculating innate lymphoid cell precursorsInnate lymphoid cellsInterleukin-23Notch signaling pathway

Identifiers

PMID41491580
PMCPMC12870510

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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.