Evidence map›Paper›PMID 31358760›Full record

ArticleNature communications2019

Activation of DR3 signaling causes loss of ILC3s and exacerbates intestinal inflammation.

Jingyu Li, Wenli Shi, Hanxiao Sun, Yan Ji, Yuqin Chen, Xiaohuan Guo, Huiming Sheng, Jie Shu, Liang Zhou, Ting Cai and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.3field-weighted citation impact, top 11% of its field
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

47 citing papers in PubMed, 61 citations in OpenAlex.

  1. A high throughput assay to identify modulators of Death Receptor 3 (DR3).SLAS discovery : advancing life sciences R & D · 2026
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  11. Frontiers in immunology · 2025
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  16. NKp46Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  17. Article
  18. Article
  19. 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

11 authors at 4 institutions in 2 countries.

Jingyu LiCAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.ORCID http://orcid.org/0000-0003-3123-6668
Wenli ShiCAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.ORCID http://orcid.org/0000-0002-4177-135X
Hanxiao SunTongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200336, China.
Yan JiCAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Yuqin ChenTongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200336, China.
Xiaohuan GuoInstitute for Immunology, Tsinghua University, Beijing, 100084, China.
Huiming ShengTongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200336, China.
Jie ShuTongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200336, China.
Liang ZhouDepartment of Infectious Diseases and Immunology, College of Veterinary Medicine, The University of Florida, Gainesville, FL, 32608, USA.
Ting CaiCAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China.
Ju QiuCAS Key Laboratory of Tissue Microenvironment and Tumor, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, 200031, China. qiuju@sibs.ac.cn.ORCID http://orcid.org/0000-0002-1543-5678
Shanghai Institute of Nutrition and Health · CNShanghai Jiao Tong University · CNTsinghua University · CNUniversity of Florida · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

TNF-like ligand 1 A (TL1A) and death receptor 3 (DR3) are a ligand-receptor pair involved in the pathogenesis of inflammatory bowel disease. Group 3 innate lymphoid cells (ILC3s) regulate intestinal immunity and highly express DR3. Here, we report that activation of DR3 signaling by an agonistic anti-DR3 antibody increases GM-CSF production from ILC3s through the p38 MAPK pathway. GM-CSF causes accumulation of eosinophils, neutrophils and CD11b

Indexed as

AnimalsAntibodiesCells, CulturedColitisEosinophilsHumansInflammatory Bowel DiseasesInterleukin-23LymphocytesMice, Inbred C57BLMice, KnockoutMice, TransgenicMyeloid CellsNeutrophilsReceptors, Tumor Necrosis Factor, Member 25Signal TransductionAntibodiesInterleukin-23Receptors, Tumor Necrosis Factor, Member 25

Identifiers

PMID31358760
PMCPMC6662828
OpenAlexW2965829044

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.