Evidence map›Paper›PMID 24868560›Full record

ArticleJournal of immunology research2014

Regulatory lymphocytes are key factors in MHC-independent resistance to EAE.

Nieves Marín, Miriam Mecha, Carmen Espejo, Leyre Mestre, Herena Eixarch, Xavier Montalban, José C Álvarez-Cermeño, Carmen Guaza, Luisa M Villar

Abstract read
In one paragraph

Article in Journal of immunology research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Influence of Housing Temperature and Genetic Diversity on Allogeneic T Cell-Induced Tissue Damage in Mice.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023
    Article
  4. Review
  5. Review
  6. 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

9 authors.

Nieves MarínMultiple Sclerosis Unit, Immunology and Neurology Departments, Hospital Universitario Ramón y Cajal, IRYCIS, Carretera de Colmenar Km 9.100, 28034 Madrid, Spain ; Red Española de Esclerosis Múltiple (REEM), RETICS, Fondo de Investigación Sanitaria, Instituto de Salud Carlos III, Ministerio de Economía y Competitividad, Madrid, Spain.
Miriam MechaRed Española de Esclerosis Múltiple (REEM), RETICS, Fondo de Investigación Sanitaria, Instituto de Salud Carlos III, Ministerio de Economía y Competitividad, Madrid, Spain ; Neuroimmunology Group, Department of Functional and System Neurobiology, Instituto Cajal, Consejo Superior de Investigaciones Científicas, Avenida Doctor Arce 37, 28002 Madrid, Spain.
Carmen EspejoRed Española de Esclerosis Múltiple (REEM), RETICS, Fondo de Investigación Sanitaria, Instituto de Salud Carlos III, Ministerio de Economía y Competitividad, Madrid, Spain ; Servei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya, Vall d'Hebron Institut de Recerca, Hospital Universitari Vall d'Hebron, Passeig de la Vall d'Hebron 119-129, 08035 Barcelona, Spain ; Universitat Autònoma de Barcelona, Bellaterra, 08193 Cerdanyola del Vallès, Spain.
Leyre MestreRed Española de Esclerosis Múltiple (REEM), RETICS, Fondo de Investigación Sanitaria, Instituto de Salud Carlos III, Ministerio de Economía y Competitividad, Madrid, Spain ; Neuroimmunology Group, Department of Functional and System Neurobiology, Instituto Cajal, Consejo Superior de Investigaciones Científicas, Avenida Doctor Arce 37, 28002 Madrid, Spain.
Herena EixarchRed Española de Esclerosis Múltiple (REEM), RETICS, Fondo de Investigación Sanitaria, Instituto de Salud Carlos III, Ministerio de Economía y Competitividad, Madrid, Spain ; Servei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya, Vall d'Hebron Institut de Recerca, Hospital Universitari Vall d'Hebron, Passeig de la Vall d'Hebron 119-129, 08035 Barcelona, Spain ; Universitat Autònoma de Barcelona, Bellaterra, 08193 Cerdanyola del Vallès, Spain.
Xavier MontalbanRed Española de Esclerosis Múltiple (REEM), RETICS, Fondo de Investigación Sanitaria, Instituto de Salud Carlos III, Ministerio de Economía y Competitividad, Madrid, Spain ; Servei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya, Vall d'Hebron Institut de Recerca, Hospital Universitari Vall d'Hebron, Passeig de la Vall d'Hebron 119-129, 08035 Barcelona, Spain ; Universitat Autònoma de Barcelona, Bellaterra, 08193 Cerdanyola del Vallès, Spain.
José C Álvarez-CermeñoMultiple Sclerosis Unit, Immunology and Neurology Departments, Hospital Universitario Ramón y Cajal, IRYCIS, Carretera de Colmenar Km 9.100, 28034 Madrid, Spain ; Universitat Autònoma de Barcelona, Bellaterra, 08193 Cerdanyola del Vallès, Spain ; Department of Medicine, Universidad de Alcalá, Plaza de San Diego s/n, Alcalá de Henares, 28801 Madrid, Spain.
Carmen GuazaRed Española de Esclerosis Múltiple (REEM), RETICS, Fondo de Investigación Sanitaria, Instituto de Salud Carlos III, Ministerio de Economía y Competitividad, Madrid, Spain ; Neuroimmunology Group, Department of Functional and System Neurobiology, Instituto Cajal, Consejo Superior de Investigaciones Científicas, Avenida Doctor Arce 37, 28002 Madrid, Spain.
Luisa M VillarMultiple Sclerosis Unit, Immunology and Neurology Departments, Hospital Universitario Ramón y Cajal, IRYCIS, Carretera de Colmenar Km 9.100, 28034 Madrid, Spain ; Red Española de Esclerosis Múltiple (REEM), RETICS, Fondo de Investigación Sanitaria, Instituto de Salud Carlos III, Ministerio de Economía y Competitividad, Madrid, Spain.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

objectivesResistant and susceptible mouse strains to experimental autoimmune encephalomyelitis (EAE), an inducible demyelinating experimental disease serving as animal model for multiple sclerosis, have been described. We aimed to explore MHC-independent mechanisms inducing resistance to EAE.

methodsFor EAE induction, female C57BL/6 (susceptible strain) and CD1 (resistant outbred strain showing heterogeneous MHC antigens) mice were immunized with the 35-55 peptide of myelin oligodendrocyte glycoprotein (MOG35-55). We studied T cell proliferation, regulatory and effector cell subpopulations, intracellular and serum cytokine patterns, and titers of anti-MOG serum antibodies.

resultsUpon immunization with MOG35-55, T lymphocytes from susceptible mice but not that of resistant strain were capable of proliferating when stimulated with MOG35-55. Accordingly, resistant mice experienced a rise in regulatory B cells (P=0.001) and, to a lower extent, in regulatory T cells (P=0.02) compared with C57BL/6 susceptible mice. As a consequence, MOG35-55-immunized C57BL/6 mice showed higher percentages of CD4+ T cells producing both IFN-gamma (P=0.02) and IL-17 (P=0.009) and higher serum levels of IL-17 (P=0.04) than resistant mice.

conclusionsExpansion of regulatory B and T cells contributes to the induction of resistance to EAE by an MHC-independent mechanism.

Indexed as

AnimalsAnimals, Outbred StrainsAntibodies, NeutralizingB-Lymphocytes, RegulatoryCell ProliferationCells, CulturedDisease SusceptibilityEncephalomyelitis, Autoimmune, ExperimentalFemaleImmunizationInterferon-gammaInterleukin-17Major Histocompatibility ComplexMiceMice, Inbred C57BLMyelin-Oligodendrocyte GlycoproteinAntibodies, NeutralizingInterferon-gammaInterleukin-17Myelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide Fragments

Identifiers

PMID24868560
PMCPMC4020375

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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.