Evidence map›Paper›PMID 22616025›Full record

ArticleScientific reports2012

Epstein-Barr virus latent membrane protein 2A exacerbates experimental autoimmune encephalomyelitis and enhances antigen presentation function.

Rhoda A Chang, Stephen D Miller, Richard Longnecker

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

10 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. Epstein-Barr Virus and Neurological Diseases.Frontiers in molecular biosciences · 2021
    Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. EBV Persistence--Introducing the Virus.Current topics in microbiology and immunology · 2015
    Review
  9. Article
  10. Evaluation of reactive Epstein-Barr Virus (EBV) in Iranian patient with different subtypes of multiple sclerosis (MS).The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases
    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

3 authors at 1 institution in 1 country.

Rhoda A ChangDepartment of Microbiology - Immunology, The Feinberg School of Medicine, Northwestern University , Chicago IL 60611, USA.
Stephen D Miller
Richard Longnecker
Northwestern University · US

Funding

Tumor Environment and Metastasis (TEAM) Research ProgramP30CA060553 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI Daniela E Matei · 1993 to 2026
$153.9M
In Vivo Model of Epstein-Barr Virus LatencyR01CA073507 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LONGNECKER, RICHARD M · 1997 to 2018
$6.1M
IMMUNOREGULATION AND PATHOLOGY OF CHRONIC-RELAPSING EAER01NS026543 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 1988 to 2016
$5.0M
Discovery of New Treatment Options for EBV-associated Lymphoma and PTLDR01CA133063 · NCI · NORTHWESTERN UNIVERSITY AT CHICAGO · PI LONGNECKER, RICHARD M · 2008 to 2012
$1.9M
Innate Regulation and CD4+Th1/17 Immunity in TMEV-Induced DemyelinationR01NS062365 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MILLER, STEPHEN D · 2010 to 2014
$1.6M
NCI NIH HHS CA133063NCI NIH HHS CA73507NCI NIH HHS P30 CA060553NCI NIH HHS R01 CA073507NCI NIH HHS R01 CA133063NINDS NIH HHS NS-026543NINDS NIH HHS NS062365NINDS NIH HHS R01 NS026543NINDS NIH HHS R01 NS062365
6 · The paper itself

Abstract

Multiple sclerosis (MS) is an inflammatory, autoimmune disease of the central nervous system. The cause of MS is still unknown but epidemiological and immunological studies have implicated Epstein-Barr virus (EBV), which infects B cells, as a possible etiological agent involved in disease. Of particular interest is EBV latent membrane protein 2A (LMP2A) because previous studies have demonstrated that LMP2A enhances the expansion and differentiation of B cells upon antigen stimulation, revealing a potential contribution of this protein in autoimmunity. Since B cells are thought to contribute to MS, we examined the role of LMP2A in the animal model experimental autoimmune encephalomyelitis (EAE). In this model, transgenic mice in which B cells express LMP2A show increased severity and incidence of disease. This difference was not due to lymphocyte recruitment into the CNS or differences in T cell activation, rather, we show that LMP2A enhances antigen presentation function.

Indexed as

Amino Acid SequenceAnimalsAntigen PresentationB-LymphocytesCell ProliferationCytokinesEncephalomyelitis, Autoimmune, ExperimentalEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryHumansImmunoglobulin GLymphocyte ActivationMaleMiceMice, Inbred C57BLCytokinesEBV-associated membrane antigen, Epstein-Barr virusImmunoglobulin GMyelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide FragmentsViral Matrix Proteins

Identifiers

PMID22616025
PMCPMC3354779
OpenAlexW2070237845

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.