Evidence map›Paper›PMID 26280015›Full record

ArticleNeurology(R) neuroimmunology & neuroinflammation2015

Macrophage migration inhibitory factor promotes resistance to glucocorticoid treatment in EAE.

Niannian Ji, Andra Kovalovsky, Günter Fingerle-Rowson, M Neal Guentzel, Thomas G Forsthuber

Open access · goldAbstract read
In one paragraph

Article in Neurology(R) neuroimmunology & neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. MIF contribution to progressive brain diseases.Journal of neuroinflammation · 2024
    Review
  5. Effects of Psychological Stress on Multiple SclerosisCNS & neurological disorders drug targets · 2024
    Review
  6. Review
  7. Brain-homing CD4Neurology(R) neuroimmunology & neuroinflammation · 2020
    Article
  8. Maize-Produced Ag2 as a Subunit Vaccine for Valley Fever.The Journal of infectious diseases · 2019
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. MIF and D-DT are potential disease severity modifiers in male MS subjects.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  14. Review
  15. Article
  16. 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

5 authors at 2 institutions in 1 country.

Niannian JiDepartment of Biology (N.J., M.N.G., T.G.F.), University of Texas at San Antonio; Department of Pathology (A.K.), Frederick Memorial Hospital, Frederick, MD; and Clinic I of Internal Medicine and Center of Integrative Oncology Cologne-Bonn (G.F.-R.), Cologne, Germany.
Andra KovalovskyDepartment of Biology (N.J., M.N.G., T.G.F.), University of Texas at San Antonio; Department of Pathology (A.K.), Frederick Memorial Hospital, Frederick, MD; and Clinic I of Internal Medicine and Center of Integrative Oncology Cologne-Bonn (G.F.-R.), Cologne, Germany.
Günter Fingerle-RowsonDepartment of Biology (N.J., M.N.G., T.G.F.), University of Texas at San Antonio; Department of Pathology (A.K.), Frederick Memorial Hospital, Frederick, MD; and Clinic I of Internal Medicine and Center of Integrative Oncology Cologne-Bonn (G.F.-R.), Cologne, Germany.
M Neal GuentzelDepartment of Biology (N.J., M.N.G., T.G.F.), University of Texas at San Antonio; Department of Pathology (A.K.), Frederick Memorial Hospital, Frederick, MD; and Clinic I of Internal Medicine and Center of Integrative Oncology Cologne-Bonn (G.F.-R.), Cologne, Germany.
Thomas G ForsthuberDepartment of Biology (N.J., M.N.G., T.G.F.), University of Texas at San Antonio; Department of Pathology (A.K.), Frederick Memorial Hospital, Frederick, MD; and Clinic I of Internal Medicine and Center of Integrative Oncology Cologne-Bonn (G.F.-R.), Cologne, Germany.
Calvert Memorial Hospital · USThe University of Texas at San Antonio · US

Funding

STRUCTURAL VISUALIZATION IN BIOINFORMATICSG12RR013646 · NCRR · UNIVERSITY OF TEXAS SAN ANTONIO · PI WENK, CAROLA · 1998 to 2011
$19.6M
Steroid resistance: Experimental Autoimmune Encephalomyelitis/Multiple SclerosisR01NS052177 · NINDS · UNIVERSITY OF TEXAS SAN ANTONIO · PI FORSTHUBER, THOMAS G. · 2007 to 2010
$1.2M
MIF inhibition as a novel treatment for autoimmune myocarditisR21AI110771 · NIAID · UNIVERSITY OF TEXAS SAN ANTONIO · PI FORSTHUBER, THOMAS G. · 2014 to 2015
$404k
NCRR NIH HHS G12 RR013646NIAID NIH HHS R21 AI110771NINDS NIH HHS R01 NS052177
6 · The paper itself

Abstract

objectiveGlucocorticoids (GCs) are used as standard treatment for acute attacks of multiple sclerosis (MS). However, GCs eventually lose efficacy and do not prevent disease progression. Macrophage migration inhibitory factor (MIF) is the only known proinflammatory cytokine induced by GCs that inhibits their anti-inflammatory effects. Therefore, we investigated whether MIF plays a role in resistance to GC treatment in experimental autoimmune encephalomyelitis (EAE), an animal model of MS.

methodsEAE was induced in wild-type (Wt) and MIF knockout (MIF(-/-)) mice followed by treatment with dexamethasone (Dex) before or upon disease onset. Splenocytes and brain mononuclear cells were harvested for cytokine ELISPOT assay and flow cytometry analysis.

resultsTreatment of EAE with Dex was substantially more efficacious in MIF(-/-) mice than Wt mice. Dex treatment decreased MOG35-55-induced cytokine production by Wt or MIF(-/-) CD4(+) T cells only at the onset of EAE but inhibited upregulation of T-bet during acute and chronic phases of disease, particularly in MIF(-/-) mice. Furthermore, passive EAE induced by adoptive transfer of T cells showed that Dex was highly effective in ameliorating disease induced by MIF(-/-) CD4(+) T cells but not by Wt CD4(+) T cells. The expression of T-bet and VLA-4 was decreased in CD4(+) T cells in MIF(-/-) mice compared with Wt mice.

conclusionsOur data establish MIF as a key molecule in resistance of pathogenic CD4(+) T cells to GC treatment in EAE and as a potential target to enhance the effectiveness of steroid treatment in neuroinflammatory disorders.

Identifiers

PMID26280015
PMCPMC4529283
OpenAlexW2159167361

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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.