Evidence map›Paper›PMID 25063874›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2014

Thiamine deficiency promotes T cell infiltration in experimental autoimmune encephalomyelitis: the involvement of CCL2.

Zhe Ji, Zhiqin Fan, Ying Zhang, Ronghuan Yu, Haihua Yang, Chenghua Zhou, Jia Luo, Zun-Ji Ke

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

22 citing papers in PubMed, 43 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 2 countries.

Zhe JiKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China;
Zhiqin FanKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China;
Ying ZhangShanghai Clinical Center, Chinese Academy of Sciences/Shanghai Xuhui Central Hospital, Shanghai 200031, China;
Ronghuan YuShanghai Clinical Center, Chinese Academy of Sciences/Shanghai Xuhui Central Hospital, Shanghai 200031, China;
Haihua YangShanghai Clinical Center, Chinese Academy of Sciences/Shanghai Xuhui Central Hospital, Shanghai 200031, China;
Chenghua ZhouKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China;
Jia LuoDepartment of Molecular and Biochemical Pharmacology, University of Kentucky College of Medicine, Lexington, KY 40536; and zunjike@yahoo.com jialuo888@uky.edu.
Zun-Ji KeKey Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China; Department of Biochemistry, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China zunjike@yahoo.com jialuo888@uky.edu.
Shanghai Xuhui Central Hospital · CNChinese Academy of Sciences · CNShanghai Institutes for Biological Sciences · CNShanghai University of Traditional Chinese Medicine · CNUniversity of Kentucky · US

Funding

GSK3BETA, A MEDIATOR OF ETHANOL NEUROTOXICITYR01AA015407 · NIAAA · WEST VIRGINIA UNIVERSITY · PI JIA LUO · 2005 to 2026
$6.2M
Autophagic Protection of Ethanol NeurotoxicityR21AA019693 · NIAAA · UNIVERSITY OF KENTUCKY · PI LUO, JIA · 2010 to 2011
$392k
NIAAA NIH HHS AA015407NIAAA NIH HHS AA019693NIAAA NIH HHS R01 AA015407NIAAA NIH HHS R21 AA019693
6 · The paper itself

Abstract

Multiple sclerosis (MS) is a complex multifactorial disease that results from the interplay between environmental factors and a susceptible genetic background. Experimental autoimmune encephalomyelitis (EAE) has been widely used to investigate the mechanisms underlying MS pathogenesis. Chemokines, such as CCL2, are involved in the development of EAE. We have previously shown that thiamine deficiency (TD) induced CCL2 in neurons. We hypothesized that TD may affect the pathogenesis of EAE. In this study, EAE was induced in C57BL/6J mice by the injection of myelin oligodendroglial glycoprotein (MOG) peptides 35-55 with or without TD. TD aggravated the development of EAE, which was indicated by clinical scores and pathologic alterations in the spinal cord. TD also accelerated the development of EAE in an adoptive transfer EAE model. TD caused microglial activation and a drastic increase (up 140%) in leukocyte infiltration in the spinal cord of the EAE mice; specifically, TD increased Th1 and Th17 cells. TD upregulated the expression of CCL2 and its receptor CCR2 in the spinal cord of EAE mice. Cells in peripheral lymph node and spleen isolated from MOG-primed TD mice showed much stronger proliferative responses to MOG. CCL2 stimulated the proliferation and migration of T lymphocytes in vitro. Our results suggested that TD exacerbated the development of EAE through activating CCL2 and inducing pathologic inflammation.

Indexed as

AnimalsCell MovementCell ProliferationChemokine CCL2Encephalomyelitis, Autoimmune, ExperimentalLymph NodesMiceMicrogliaMyelin-Oligodendrocyte GlycoproteinPeptide FragmentsRatsSpinal CordSpleenTh17 CellsTh1 CellsThiamine DeficiencyCcl2 protein, mouseChemokine CCL2Myelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide Fragments

Identifiers

PMID25063874
PMCPMC4135011
OpenAlexW2145777551

What OpenQuestion holds

Textmetadata
LicenceTDM
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.