Evidence map›Paper›PMID 40781334›Full record

ArticleJournal of neuroinflammation2025

CRTH2 is critical for IL-1β-producing B cells during experimental autoimmune encephalomyelitis in mice via p38 signaling.

Jiao Liu, Bei Wang, Chunyan Wu, Ting Wang, Jie Zhou, Yujun Shen, Ying Yu, Shengkai Zuo

Abstract read
In one paragraph

Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

8 authors.

Jiao Liu *Department of Pharmacology, Tianjin Key Laboratory of Inflammatory Biology, Center for Cardiovascular Diseases, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, State Key Laboratory of Experimental Hematology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Bei Wang *Department of Pharmacology, Tianjin Key Laboratory of Inflammatory Biology, Center for Cardiovascular Diseases, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, State Key Laboratory of Experimental Hematology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Chunyan WuDepartment of Biopharmaceutics, School of Pharmacy, Tianjin Medical University, Tianjin, China.
Ting WangDepartment of Biopharmaceutics, School of Pharmacy, Tianjin Medical University, Tianjin, China.
Jie ZhouDepartment of Immunology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Yujun ShenDepartment of Pharmacology, Tianjin Key Laboratory of Inflammatory Biology, Center for Cardiovascular Diseases, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, State Key Laboratory of Experimental Hematology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China.
Ying YuDepartment of Pharmacology, Tianjin Key Laboratory of Inflammatory Biology, Center for Cardiovascular Diseases, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, State Key Laboratory of Experimental Hematology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China. yuying@tmu.edu.cn.
Shengkai ZuoDepartment of Pharmacology, Tianjin Key Laboratory of Inflammatory Biology, Center for Cardiovascular Diseases, Key Laboratory of Immune Microenvironment and Disease (Ministry of Education), The Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, State Key Laboratory of Experimental Hematology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China. zuoshengkai@tmu.edu.cn.

Funding

National Natural Science Foundation of China 82030015National Natural Science Foundation of China 82171792
6 · The paper itself

Abstract

B cells play a critical role in the pathogenesis of autoimmune inflammatory diseases such as multiple sclerosis (MS). As a receptor of prostaglandin D

Indexed as

B-LymphocytesEncephalomyelitis, Autoimmune, ExperimentalInterleukin-1betaMAP Kinase Signaling Systemp38 Mitogen-Activated Protein KinasesReceptors, ImmunologicReceptors, ProstaglandinAnimalsFemaleMiceMice, Inbred C57BLMice, KnockoutPeptide FragmentsSignal TransductionInterleukin-1betap38 Mitogen-Activated Protein KinasesPeptide Fragmentsprostaglandin D2 receptorReceptors, ImmunologicReceptors, ProstaglandinB cellsCRTH2Experimental autoimmune encephalomyelitisIL-1βp38 MAPK signaling

Identifiers

PMID40781334
PMCPMC12335081

What OpenQuestion holds

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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.