Evidence map›Paper›PMID 30671738›Full record

ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2019

Protective effects of CX3CR1 on autoimmune inflammation in a chronic EAE model for MS through modulation of antigen-presenting cell-related molecular MHC-II and its regulators.

Weihua Mai, Xingwei Liu, Junfeng Wang, Jing Zheng, Xiao Wang, Wenying Zhou

Abstract read
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In one paragraph

Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.1field-weighted citation impact, top 49% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Deletion of the X-chromosomal geneScience translational medicine · 2025
    Article
  3. Review
  4. Article
  5. CXInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023
    Article
  6. Article
  7. 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

6 authors at 1 institution in 1 country.

Weihua MaiDepartment of Neurology, The Fifth Affiliated Hospital of Sun Yat-sen University, NO. 52 East Meihua Road, Zhuhai, 519000, Guangdong Province, China. weihuamai2004@163.com.ORCID http://orcid.org/0000-0002-3328-4236
Xingwei LiuDepartment of General Surgery, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China.
Junfeng WangDepartment of Neurology, The Fifth Affiliated Hospital of Sun Yat-sen University, NO. 52 East Meihua Road, Zhuhai, 519000, Guangdong Province, China.
Jing ZhengDepartment of Nephrology, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China.
Xiao WangDepartment of General Surgery, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China.
Wenying ZhouDepartment of Laboratory Science, The Fifth Affiliated Hospital of Sun Yat-sen University, Zhuhai, China.
Sun Yat-sen University · CN

Funding

Natural Science Foundation of Guangdong Province, China 2014A030313028Science and Technology Planning Project of Zhuhai city, China 2015A1011
6 · The paper itself

Abstract

backgroundRecent evidences have implicated neuroprotective effects of CX3CR1 in multiple sclerosis (MS). But whether CX3CR1 is involved in modulation of antigen-presenting cell (APC)-related molecular MHC-II and what the possible mechanism is remain unidentified.

objectiveIn this study, we intended to investigate the effects of CX3CR1 on MHC-II expressions on brain myeloid cells in experimental autoimmune encephalomyelitis (EAE) mice and explore the possible regulators for it.

methodsCX3CR1-deficient EAE mice were created. Disease severity, pathological damage, and the expressions of MHC-II and its mediators on myeloid cells were detected.

resultsWe found that compare with wile-typed EAE mice, CX3CR1-deficient EAE mice exhibited more severe disease severity. An accumulation of CD45

conclusionsThe findings indicated that CX3CR1 might be an important regulator for MHC-II expressions on APCs, playing a beneficial role in EAE. The mechanism was probably through regulation on the MHC-II regulators CIITA and IRF-1.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalInflammationMultiple SclerosisAnimalsAntigen-Presenting CellsCX3C Chemokine Receptor 1Disease Models, AnimalFemaleHistocompatibility Antigens Class IIInterferon Regulatory Factor-1MiceMice, Inbred C57BLMyeloid CellsNuclear ProteinsTrans-ActivatorsCX3C Chemokine Receptor 1Cx3cr1 protein, mouseHistocompatibility Antigens Class IIInterferon Regulatory Factor-1Irf1 protein, mouseMHC class II transactivator proteinNuclear ProteinsTrans-ActivatorsClass II transactivatorCX3CR1Experimental autoimmune encephalomyelitisInterferon regulatory factor-1Major histocompatibility complex class II moleculesMultiple sclerosis

Identifiers

PMID30671738
OpenAlexW2914473053

What OpenQuestion 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 OpenQuestion graph.