Evidence map›Paper›PMID 39741194›Full record

ArticleCellular & molecular immunology2025

NRP1 instructs IL-17-producing ILC3s to drive colitis progression.

Ying Wang, Jianye Wang, Gaoyu Liu, Xianfu Yi, Jingyi Wu, Hailong Cao, Lijuan Zhang, Pan Zhou, Yong Fan, Ying Yu and 4 more

Abstract read
In one paragraph

Article in Cellular & molecular immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

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  11. [Construction of a highly efficient HBV infection cell model based on HBV co-receptor neuropilin-1].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2025
    Article
  12. Article
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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

14 authors.

Ying Wang *Department of oncology, The Second Hospital of Tianjin Medical University; Tianjin Key Laboratory of Precision Medicine for Sex Hormones and Diseases; Tianjin Institute of Immunology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Jianye Wang *Department of oncology, The Second Hospital of Tianjin Medical University; Tianjin Key Laboratory of Precision Medicine for Sex Hormones and Diseases; Tianjin Institute of Immunology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Gaoyu Liu *Department of oncology, The Second Hospital of Tianjin Medical University; Tianjin Key Laboratory of Precision Medicine for Sex Hormones and Diseases; Tianjin Institute of Immunology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Xianfu YiDepartment of Bioinformatics, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Jingyi WuDepartment of Gastroenterology and Hepatology, General Hospital, Tianjin Medical University, Tianjin, China.
Hailong CaoDepartment of Gastroenterology and Hepatology, General Hospital, Tianjin Medical University, Tianjin, China.
Lijuan ZhangDepartment of oncology, The Second Hospital of Tianjin Medical University; Tianjin Key Laboratory of Precision Medicine for Sex Hormones and Diseases; Tianjin Institute of Immunology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Pan ZhouDepartment of oncology, The Second Hospital of Tianjin Medical University; Tianjin Key Laboratory of Precision Medicine for Sex Hormones and Diseases; Tianjin Institute of Immunology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Yong FanKey Laboratory for Major Obstetric Diseases of Guangdong Province, Center of Reproductive Medicine, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Ying YuDepartment of Pharmacology, Tianjin Key Laboratory of Inflammatory Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.ORCID 0000-0002-6476-1752
Qiang LiuDepartment of Neurology, Tianjin Neurological Institute, Tianjin Institute of Immunology, Tianjin Medical University General Hospital, Tianjin, China.
Zhi YaoDepartment of oncology, The Second Hospital of Tianjin Medical University; Tianjin Key Laboratory of Precision Medicine for Sex Hormones and Diseases; Tianjin Institute of Immunology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Haitao WangDepartment of oncology, The Second Hospital of Tianjin Medical University; Tianjin Key Laboratory of Precision Medicine for Sex Hormones and Diseases; Tianjin Institute of Immunology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China. peterrock2000@vip.126.com.
Jie ZhouDepartment of oncology, The Second Hospital of Tianjin Medical University; Tianjin Key Laboratory of Precision Medicine for Sex Hormones and Diseases; Tianjin Institute of Immunology, Department of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China. zhoujie@tmu.edu.cn.ORCID 0000-0001-5964-1599

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81925018National Natural Science Foundation of China (National Science Foundation of China) 82130049National Natural Science Foundation of China (National Science Foundation of China) 82225015National Natural Science Foundation of China (National Science Foundation of China) 82321001
6 · The paper itself

Abstract

Group 3 innate lymphoid cells (ILC3s) control tissue homeostasis and orchestrate mucosal inflammation; however, the precise mechanisms governing ILC3 activity are fully understood. Here, we identified the transmembrane protein neuropilin-1 (NRP1) as a positive regulator of interleukin (IL)-17-producing ILC3s in the intestine. NRP1 was markedly upregulated in intestinal mucosal biopsies from patients with inflammatory bowel disease (IBD) compared with healthy controls. Genetic deficiency of NRP1 reduces the frequency of ILC3s in the gut and impairs their production of IL-17A in an NF-κB signaling-dependent and cell-intrinsic manner. The diminished IL-17A production in ILC3s altered the composition of the microbiota and improved the outcome of dextran sodium sulfate (DSS)-induced colitis. Furthermore, pharmacological inhibition of NRP1 with EG00229 alleviated the severity of colitis. These observations demonstrated the critical role of NRP1 in the control of intestinal ILC3s, suggesting that NRP1 is a potential therapeutic target for IBD.

Indexed as

ColitisDisease ProgressionInterleukin-17LymphocytesNeuropilin-1AnimalsDextran SulfateFemaleHumansImmunity, InnateIntestinal MucosaMaleMiceMice, Inbred C57BLMice, KnockoutNF-kappa BDextran SulfateInterleukin-17Neuropilin-1NF-kappa BNRP1 protein, humanGroup 3 innate lymphoid cells (ILC3s)Inflammatory bowel disease (IBD)Mucosal ImmunityNRP1

Identifiers

PMID39741194
PMCPMC11782674

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 Socratic graph.