Evidence map›Paper›PMID 38528529›Full record

ArticleJournal of neuroinflammation2024

P2X7 receptor antagonists modulate experimental autoimmune neuritis via regulation of NLRP3 inflammasome activation and Th17 and Th1 cell differentiation.

Yuhan Xie, Ranran Han, Yulin Li, Weiya Li, Shichao Zhang, Yu Wu, Yuexin Zhao, Rongrong Liu, Jie Wu, Wei Jiang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

17 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  4. The EGR1/ZFP36 axis governs glycosphingolipid metabolic reprogramming in monocyte-derived macrophages in guillain-barré syndrome.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
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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 5 institutions in 1 country.

Yuhan Xie *Department of Neurology, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, 300052, China.
Ranran Han *Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Yulin Li *Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Weiya Li *Department of Neurology, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, 300052, China.
Shichao ZhangDepartment of Urology, Tianjin Institute of Urology, The Second Hospital of Tianjin Medical University, Tianjin, 300102, China.
Yu WuDepartment of Neurology, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, 300052, China.
Yuexin ZhaoDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Rongrong LiuDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Jie WuDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China.
Wei JiangDepartment of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, 300052, China. jiangwei.med@gmail.com.
Xiuju ChenDepartment of Neurology, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, 300052, China. chyjutj@163.com.
Tianjin Medical University General Hospital · CNTianjin Medical University · CNSecond Hospital of Tianjin Medical University · CNThird Affiliated Hospital of Zhengzhou University · CNTianjin Nankai Hospital · CN

Funding

National Natural Science Foundation of China 82001280National Natural Science Foundation of China 82171277National Natural Science Foundation of China 82301523
6 · The paper itself

Abstract

backgroundGuillain-Barré syndrome (GBS), a post-infectious, immune-mediated, acute demyelinating disease of the peripheral nerves and nerve roots, represents the most prevalent and severe acute paralyzing neuropathy. Purinergic P2X7 receptors (P2X7R) play a crucial role in central nervous system inflammation. However, little is known about their role in the immune-inflammatory response within the peripheral nervous system.

methodsInitially, we assessed the expression of purinergic P2X7R in the peripheral blood of patients with GBS using flow cytometry and qRT-PCR. Next, we explored the expression of P2 X7R in CD4

resultsP2X7R expression was elevated not only in the peripheral blood of patients with GBS but also in rats with EAN. In rats with EAN, inhibiting P2X7R with BBG alleviated neurological symptoms, reduced demyelination, decreased inflammatory cell infiltration of the peripheral nerves, and improved nerve conduction. BBG also limited the production of pro-inflammatory molecules, down-regulated the expression of P2X7R and NLRP3, and suppressed the differentiation of Th1 and Th17 cells, thus protecting against EAN. These effects collectively contribute to modifying the inflammatory environment and enhancing outcomes in EAN rats.

conclusionsSuppression of P2X7R relieved EAN manifestation by regulating CD4

Indexed as

Guillain-Barre SyndromeNeuritis, Autoimmune, ExperimentalPurinergic P2X Receptor AntagonistsAnimalsCD8-Positive T-LymphocytesCell DifferentiationHumansInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinRatsSciatic NerveTh17 CellsTh1 CellsInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinPurinergic P2X Receptor AntagonistsBrilliant blue GCD4+ T cellGuillain–Barré syndromeP2X7R

Identifiers

PMID38528529
PMCPMC10964508
OpenAlexW4393161334

What OpenQuestion holds

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LicenceCC BY
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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.