Evidence map›Paper›PMID 40765112›Full record

ArticleCNS neuroscience & therapeutics2025

The Quinazoline Derivative, QNZ, Alleviates Experimental Autoimmune Encephalomyelitis by Suppressing Th1 and Th17 Cells.

Fan Yang, Yuan Yang, Gan Zhang, Juan Li, Shan Chen, Yan Zhou, Yuhang Kong, Xingyan Luo, Yang Liu, Ying Xu and 1 more

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Article
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.

Fan YangClinical Laboratory, Clinical Medical College and The First Affiliated Hospital of Chengdu Medical College, Chengdu Medical College, Chengdu, Sichuan, China.
Yuan YangDepartment of Rheumatology and Immunology, Clinical Medical College and The First Affiliated Hospital of Chengdu Medical College, Chengdu Medical College, Chengdu, Sichuan, China.
Gan ZhangClinical Laboratory, Clinical Medical College and The First Affiliated Hospital of Chengdu Medical College, Chengdu Medical College, Chengdu, Sichuan, China.
Juan LiClinical Laboratory, Clinical Medical College and The First Affiliated Hospital of Chengdu Medical College, Chengdu Medical College, Chengdu, Sichuan, China.
Shan ChenClinical Laboratory, Clinical Medical College and The First Affiliated Hospital of Chengdu Medical College, Chengdu Medical College, Chengdu, Sichuan, China.
Yan ZhouDepartment of Emergency, West China Second University Hospital, Sichuan University, Chengdu, Sichuan, China.
Yuhang KongClinical Laboratory, Clinical Medical College and The First Affiliated Hospital of Chengdu Medical College, Chengdu Medical College, Chengdu, Sichuan, China.
Xingyan LuoClinical Laboratory, Clinical Medical College and The First Affiliated Hospital of Chengdu Medical College, Chengdu Medical College, Chengdu, Sichuan, China.ORCID 0000-0002-7478-1984
Yang LiuClinical Laboratory, Clinical Medical College and The First Affiliated Hospital of Chengdu Medical College, Chengdu Medical College, Chengdu, Sichuan, China.
Ying XuClinical Laboratory, Clinical Medical College and The First Affiliated Hospital of Chengdu Medical College, Chengdu Medical College, Chengdu, Sichuan, China.ORCID 0000-0001-9570-8666
Yantang WangClinical Laboratory, Clinical Medical College and The First Affiliated Hospital of Chengdu Medical College, Chengdu Medical College, Chengdu, Sichuan, China.ORCID 0000-0003-0854-4988

Funding

CMC Excellent-talent Program 2024kjTzn04Disciplinary Construction Innovation Team Foundation of Chengdu Medical College CMC-XK-2103National Natural Science Foundation of China 81871300Natural Science Foundation of Sichuan Province 2025NSFSC2253Research Fund of Development and Regeneration Key Laboratory of Sichuan Province 24FYYZ507
6 · The paper itself

Abstract

aimsMultiple Sclerosis (MS) is a neuroinflammatory and neurodegenerative disease affecting the central nervous system (CNS). Substantial evidence implicates a central role for CD4+ T cells in MS pathogenesis, particularly IFN-γ+ Th1 cells and IL-17+ Th17 cells. NF-κB plays an essential role in regulating the differentiation of Th1 and Th17 cells, which typically mediate inflammatory responses as self-triggers. QNZ is a highly selective inhibitor of NF-κB transcriptional activation. In this study, we assessed the impact of QNZ on CD4+ T-cell polarization in MS. Utilizing the experimental autoimmune encephalomyelitis (EAE) model, we investigated these aspects of MS.

methodEAE was induced in C57BL/6 female mice by active immunization with myelin oligodendrocyte glycoprotein (MOG)

resultsProphylactic administration of QNZ to EAE mice suppressed the differentiation of Th1 and Th17 cells and demyelination within the spinal cord. Notably, QNZ also reduced the proportion of IFN-γ+IL-17+ Th17.1 cells, potentially playing a critical role in MS pathogenesis.

conclusionsQuinazoline derivative QNZ could suppress neuroinflammation, alleviate the progression of EAE and be associated with reduced Th1 and Th17 immunity.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalQuinazolinesTh17 CellsTh1 CellsAnimalsFemaleMiceMice, Inbred C57BLQuinazolinesexperimental autoimmune encephalomyelitismultiple sclerosisneuroinflammationQNZTh17.1 cellsTh17 cells

Identifiers

PMID40765112
PMCPMC12325097

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Registered trials

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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.