Evidence map›Paper›PMID 22488447›Full record

ReviewSeminars in immunopathology2012

Pathogenesis of multiple sclerosis via environmental and genetic dysregulation of N-glycosylation.

Ani Grigorian, Haik Mkhikian, Carey F Li, Barbara L Newton, Raymond W Zhou, Michael Demetriou

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in immunopathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

21 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Extracellular matrix protein N-glycosylation mediates immune self-tolerance inProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  7. Establishing Rules for Self-Adhesion and Aggregation ofLangmuir : the ACS journal of surfaces and colloids · 2020
    Article
  8. Article
  9. Article
  10. Review
  11. Frontiers in immunology · 2019
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Ani GrigorianInstitute for Immunology, Department of Neurology, University of California, Irvine, Irvine, CA 92697, USA.
Haik Mkhikian
Carey F Li
Barbara L Newton
Raymond W Zhou
Michael Demetriou
University of California, Irvine · US

Funding

T cell regulation by N-glycosylationR01AI053331 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI DEMETRIOU, MICHAEL · 2003 to 2014
$3.5M
Human Autoimmunity and Genetic Defects in N-GlycosylationR01AI082266 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI DEMETRIOU, MICHAEL · 2010 to 2013
$1.5M
N-glycosylation as a downstream effector of Interleukin-7F30HL108451 · NHLBI · UNIVERSITY OF CALIFORNIA-IRVINE · PI MKHIKIAN, HAIK · 2011 to 2015
$202k
Vitamin D3, Autoimmunity and N-glycosylationF32AI081456 · NIAID · UNIVERSITY OF CALIFORNIA-IRVINE · PI OGANESYAN, ANI · 2009 to 2010
$98k
NHLBI NIH HHS F30 HL108451NIAID NIH HHS F32 AI081456NIAID NIH HHS F32AI081456NIAID NIH HHS R01 AI053331NIAID NIH HHS R01AI053331NIAID NIH HHS R01 AI082266NIAID NIH HHS R01AI082266
6 · The paper itself

Abstract

Autoimmune diseases such as multiple sclerosis (MS) result from complex and poorly understood interactions of genetic and environmental factors. A central role for T cells in MS is supported by mouse models, association of the major histocompatibility complex region, and association of critical T cell growth regulator genes such as interleukin-2 receptor (IL-2RA) and interleukin-7 receptor (IL-7RA). Multiple environmental factors (vitamin D(3) deficiency and metabolism) converge with multiple genetic variants (IL-7RA, IL-2RA, MGAT1, and CTLA-4) to dysregulate Golgi N-glycosylation in MS, resulting in T cell hyperactivity, loss of self-tolerance and in mice, a spontaneous MS-like disease with neurodegeneration. Here, we review the genetic and biological interactions that regulate MS pathogenesis through dysregulation of N-glycosylation and how this may enable individualized therapeutic approaches.

Indexed as

AutoimmunityAcyltransferasesAnimalsCTLA-4 AntigenGlycosylationHumansInterleukin-2 Receptor alpha SubunitMiceMice, Inbred C57BLMultiple SclerosisN-AcetylglucosaminyltransferasesReceptors, Interleukin-7T-LymphocytesAcyltransferasesCTLA-4 AntigenInterleukin-2 Receptor alpha Subunitinterleukin-7 receptor, alpha chainMGAT1 protein, mouseN-AcetylglucosaminyltransferasesReceptors, Interleukin-7

Identifiers

PMID22488447
PMCPMC3960996
OpenAlexW1994245422

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.