Evidence map›Paper›PMID 26142251›Full record

ReviewJournal of autoimmunity2015

The immunogenetics of multiple sclerosis: A comprehensive review.

Jill A Hollenbach, Jorge R Oksenberg

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of autoimmunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 196 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
196citing papers in PubMed, 3 pooled it
12.2field-weighted citation impact, top 1% 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

196 citing papers in PubMed, 3 syntheses or guidelines pooled it, 401 citations in OpenAlex.

  1. Pooled it
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  3. Pooled it
  4. Trial
  5. Molecular mimicry between Anoctamin 2 and Epstein-Barr virus nuclear antigen 1 associates with multiple sclerosis risk.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Trial
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136 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Jill A HollenbachDepartment of Neurology, University of California San Francisco, San Francisco, CA 94158, USA. Electronic address: jill.hollenbach@ucsf.edu.
Jorge R OksenbergDepartment of Neurology, University of California San Francisco, San Francisco, CA 94158, USA.
University of California, San Francisco · US

Funding

The contribution of common and rare variants to autoimmunity in African AmericansR01NS076492 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI OKSENBERG, JORGE R. · 2011 to 2014
$1.3M
Integrated Exchange & Storage of Current and Future-Generation Immunogenomic DataR01GM109030 · NIGMS · CHILDREN'S HOSPITAL & RES CTR AT OAKLAND · PI HOLLENBACH, JILL ALLISON, MACK, STEVEN JOHN · 2014 to 2016
$919k
NIGMS NIH HHS R01 GM109030NINDS NIH HHS R01 NS076492
6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system and common cause of non-traumatic neurological disability in young adults. The likelihood for an individual to develop MS is strongly influenced by her or his ethnic background and family history of disease, suggesting that genetic susceptibility is a key determinant of risk. Over 100 loci have been firmly associated with susceptibility, whereas the main signal genome-wide maps to the class II region of the human leukocyte antigen (HLA) gene cluster and explains up to 10.5% of the genetic variance underlying risk. HLA-DRB1*15:01 has the strongest effect with an average odds ratio of 3.08. However, complex allelic hierarchical lineages, cis/trans haplotypic effects, and independent protective signals in the class I region of the locus have been described as well. Despite the remarkable molecular dissection of the HLA region in MS, further studies are needed to generate unifying models to account for the role of the MHC in disease pathogenesis. Driven by the discovery of combinatorial associations of Killer-cell Immunoglobulin-like Receptor (KIR) and HLA alleles with infectious, autoimmune diseases, transplantation outcome and pregnancy, multi-locus immunogenomic research is now thriving. Central to immunity and critically important for human health, KIR molecules and their HLA ligands are encoded by complex genetic systems with extraordinarily high levels of sequence and structural variation and complex expression patterns. However, studies to-date of KIR in MS have been few and limited to very low resolution genotyping. Application of modern sequencing methodologies coupled with state of the art bioinformatics and analytical approaches will permit us to fully appreciate the impact of HLA and KIR variation in MS.

Indexed as

ImmunogeneticsAllelesAnimalsGenetic Association StudiesGenetic Predisposition to DiseaseGenetic VariationHLA AntigensHumansMultiple SclerosisHLA AntigensGeneticsHuman leukocyte antigenKiller-cell immunoglobulin-like receptorMultiple sclerosis

Identifiers

PMID26142251
PMCPMC4687745
OpenAlexW775956452

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.