Evidence map›Paper›PMID 19912648›Full record

ArticleJournal of neuroinflammation2009

Modulation of experimental autoimmune encephalomyelitis by endogenous annexin A1.

Nikolaos Paschalidis, Asif J Iqbal, Francesco Maione, Elisabeth G Wood, Mauro Perretti, Rod J Flower, Fulvio D'Acquisto

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.5field-weighted citation impact, top 33% 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

24 citing papers in PubMed, 52 citations in OpenAlex.

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  10. Tamoxifen induces apoptotic neutrophil efferocytosis in horses.Veterinary research communications · 2018
    Article
  11. Anti-inflammatory effects of hypoxia-preconditioned human periodontal ligament cell secretome in an experimental model of multiple sclerosis: a key role of IL-37.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
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  19. Endogenous galectin-1 exerts tonic inhibition on experimental arthritis.Journal of immunology (Baltimore, Md. : 1950) · 2013
    Article
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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

7 authors at 2 institutions in 1 country.

Nikolaos PaschalidisWilliam Harvey Research Institute, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M6BQ, UK.
Asif J Iqbal
Francesco Maione
Elisabeth G Wood
Mauro Perretti
Rod J Flower
Fulvio D'Acquisto
Queen Mary University of London · GBWilliam Harvey Research Institute · GB

Funding

Medical Research Council G0400327Multiple Sclerosis Society 860
6 · The paper itself

Abstract

backgroundAutoimmune diseases, like multiple sclerosis, are triggered by uncontrolled activation of cells of the immune system against self-antigen present, for instance, in the central nervous system. We have reported novel biological functions for Annexin A1, an effector of endogenous anti-inflammation, to produce positive actions on the adaptive immune system by reducing the threshold of T cell activation. In this study, we investigated the potential modulatory role of Annexin A1 in the development of experimental autoimmune encephalomyelitis, a model of multiple sclerosis.

methodsMale control C57/BL6 and AnxA1 null mice were immunized subcutaneously with an emulsion consisting of 300 microg of MOG35-55 in PBS combined with an equal volume of CFA. Lymph node cells obtained from mice immunized with MOG33-55 for 14 days were re-stimulated in vitro with MOG33-55 (100 microg/ml) for 4 days and the Th1/Th17 cytokine profile measured by ELISA. Spinal cords were processed either to isolate the infiltrated T cells or fixed and stained with haematoxylin and eosin. Statistical analyses were performed using two-tailed, unpaired Student's t tests or ANOVA.

resultsOur results show a direct correlation between Annexin A1 expression and severity of EAE. Analysis of MOG35-55-induced EAE development in Annexin A1 null mice showed decreased signs of the disease compared to wild type mice. This defect was significant at the peak of the disease and accompanied by reduced infiltration of T cells in the spinal cord. Finally, analysis of the T cell recall response in vitro following stimulation with MOG35-55 showed a decrease proliferation of Annexin A1 null T cells, with a significantly reduced Th1/Th17 phenotype, compared to wild type cells.

conclusionTogether these findings suggest that Annexin A1 null mice have an impaired capacity to develop EAE. Furthermore strategies aiming at reducing Annexin A1 functions or expression in T cells might represent a novel therapeutic approach for multiple sclerosis.

Indexed as

AnimalsAnnexin A1Cell ProliferationCytokinesEncephalomyelitis, Autoimmune, ExperimentalGlycoproteinsLymph NodesLymphocyte SubsetsMaleMiceMice, Inbred C57BLMice, KnockoutMyelin-Oligodendrocyte GlycoproteinPeptide FragmentsSpinal CordTh1 CellsAnnexin A1CytokinesGlycoproteinsMyelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide Fragments

Identifiers

PMID19912648
PMCPMC2780380
OpenAlexW2170240315

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.