Evidence map›Paper›PMID 26274821›Full record

SynthesisPloS one2015

Influence of the LILRA3 Deletion on Multiple Sclerosis Risk: Original Data and Meta-Analysis.

Miguel A Ortiz, Concepción Núñez, David Ordóñez, José C Alvarez-Cermeño, José E Martínez-Rodriguez, Antonio J Sánchez, Rafael Arroyo, Guillermo Izquierdo, Sunny Malhotra, Xavier Montalban and 7 more

Open access · goldAbstract readMeta-Analysis
In one paragraph

Synthesis in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.1field-weighted citation impact, top 47% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Frequencies of theFrontiers in genetics · 2019
    Article
  2. 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

17 authors at 7 institutions in 1 country.

Miguel A OrtizImmunology Department, Hospital Clínico San Carlos, Instituto de Investigación Sanitaria San Carlos (IdISSC), Madrid, Spain.
Concepción NúñezImmunology Department, Hospital Clínico San Carlos, Instituto de Investigación Sanitaria San Carlos (IdISSC), Madrid, Spain.
David OrdóñezImmunogenetics & Histocompatibility, Instituto de Investigación Sanitaria Puerta de Hierro, Majadahonda, Madrid, Spain.
José C Alvarez-CermeñoDepartments of Immunology and Neurology, Multiple Sclerosis Unit, Hospital Ramon y Cajal, (IRYCIS), Madrid, Spain.
José E Martínez-RodriguezNeurology, Hospital del Mar Medical Research Institute (IMIM), Barcelona, Spain.
Antonio J SánchezNeuroimmunology, Hospital Universitario Puerta de Hierro, Majadahonda, Madrid, Spain.
Rafael ArroyoMultiple Sclerosis Unit, Neurology Department. Hospital Clínico S. Carlos, Instituto de Investigación Sanitaria S. Carlos (IdISSC), Madrid, Spain.
Guillermo IzquierdoMultiple Sclerosis Unit, Hospital Virgen Macarena, Sevilla, Spain.
Sunny MalhotraServei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d'Hebron (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
Xavier MontalbanServei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d'Hebron (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
Antonio García-MerinoNeuroimmunology, Hospital Universitario Puerta de Hierro, Majadahonda, Madrid, Spain.
Elvira MunteisNeurology, Hospital del Mar Medical Research Institute (IMIM), Barcelona, Spain.
Antonio AlcinaDepartment of Cell Biology and Immunology, Instituto de Parasitología y Biomedicina "López Neyra", Consejo Superior de Investigaciones Científicas (IPBLN-CSIC), Granada, Spain.
Manuel ComabellaServei de Neurologia-Neuroimmunologia, Centre d'Esclerosi Múltiple de Catalunya (Cemcat), Institut de Recerca Vall d'Hebron (VHIR), Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
Fuencisla MatesanzDepartment of Cell Biology and Immunology, Instituto de Parasitología y Biomedicina "López Neyra", Consejo Superior de Investigaciones Científicas (IPBLN-CSIC), Granada, Spain.
Luisa M VillarDepartments of Immunology and Neurology, Multiple Sclerosis Unit, Hospital Ramon y Cajal, (IRYCIS), Madrid, Spain.
Elena UrcelayImmunology Department, Hospital Clínico San Carlos, Instituto de Investigación Sanitaria San Carlos (IdISSC), Madrid, Spain.
Instituto de Investigación Sanitaria del Hospital Clínico San Carlos · ESHospital Universitario Puerta de Hierro Majadahonda · ESUniversitat Autònoma de Barcelona · ESConsejo Superior de Investigaciones Científicas · ESHospital Del Mar · ESInstituto Ramón y Cajal de Investigación Sanitaria · ESHospital Universitario Virgen Macarena · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMultiple sclerosis (MS) is a neurodegenerative, autoimmune disease of the central nervous system. Genome-wide association studies (GWAS) have identified over hundred polymorphisms with modest individual effects in MS susceptibility and they have confirmed the main individual effect of the Major Histocompatibility Complex. Additional risk loci with immunologically relevant genes were found significantly overrepresented. Nonetheless, it is accepted that most of the genetic architecture underlying susceptibility to the disease remains to be defined. Candidate association studies of the leukocyte immunoglobulin-like receptor LILRA3 gene in MS have been repeatedly reported with inconsistent results.

objectivesIn an attempt to shed some light on these controversial findings, a combined analysis was performed including the previously published datasets and three newly genotyped cohorts. Both wild-type and deleted LILRA3 alleles were discriminated in a single-tube PCR amplification and the resulting products were visualized by their different electrophoretic mobilities. RESULTS AND

conclusionOverall, this meta-analysis involved 3200 MS patients and 3069 matched healthy controls and it did not evidence significant association of the LILRA3 deletion [carriers of LILRA3 deletion: p = 0.25, OR (95% CI) = 1.07 (0.95-1.19)], even after stratification by gender and the HLA-DRB1*15:01 risk allele.

Indexed as

Gene DeletionEpistasis, GeneticGenetic Association StudiesGenetic Predisposition to DiseaseHLA-DRB1 ChainsHumansMultiple SclerosisReceptors, ImmunologicWhite PeopleHLA-DRB1*15:01 antigenHLA-DRB1 ChainsLILRA3 protein, humanReceptors, Immunologic

Identifiers

PMID26274821
PMCPMC4537248
OpenAlexW2130265004

What OpenQuestion holds

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LicenceCC BY
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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.