Evidence map›Paper›PMID 26610735›Full record

ArticleThe Journal of infectious diseases2016

Genetic Variation in Toll-Interacting Protein Is Associated With Leprosy Susceptibility and Cutaneous Expression of Interleukin 1 Receptor Antagonist.

Javeed A Shah, William R Berrington, James C Vary, Richard D Wells, Glenna J Peterson, Chhatra B Kunwar, Saraswoti Khadge, Deanna A Hagge, Thomas R Hawn

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  7. Pathogenic Single Nucleotide Polymorphisms on Autophagy-Related Genes.International journal of molecular sciences · 2020
    Review
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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 at 2 institutions in 2 countries.

Javeed A ShahUniversity of Washington School of Medicine, Seattle, Washington.
William R BerringtonUniversity of Washington School of Medicine, Seattle, Washington.
James C VaryUniversity of Washington School of Medicine, Seattle, Washington Puget Sound VA Health Care System, Seattle, Washington.
Richard D WellsUniversity of Washington School of Medicine, Seattle, Washington.
Glenna J PetersonUniversity of Washington School of Medicine, Seattle, Washington.
Chhatra B KunwarMycobacterial Research Laboratories, Anandaban Hospital, Kathmandu, Nepal.
Saraswoti KhadgeMycobacterial Research Laboratories, Anandaban Hospital, Kathmandu, Nepal.
Deanna A HaggeMycobacterial Research Laboratories, Anandaban Hospital, Kathmandu, Nepal.
Thomas R HawnUniversity of Washington School of Medicine, Seattle, Washington.
University of Washington · USAnandaban Hospital · NP

Funding

Innate Immunogenetics & Human InfectionsK24AI089794 · NIAID · UNIVERSITY OF WASHINGTON · PI HAWN, THOMAS R · 2010 to 2014
$746k
TOLLIP and Tuberculosis ImmunopathogenesisK08AI102971 · NIAID · UNIVERSITY OF WASHINGTON · PI SHAH, JAVEED ALI · 2013 to 2016
$708k
The Role of Nod1 and Nod2 in the Pathogeneisis of Legionella Pneumophila PneumoniK08AI080952 · NIAID · UNIVERSITY OF WASHINGTON · PI BERRINGTON, WILLIAM RICHARD · 2009 to 2012
$623k
NIAID NIH HHS K08 AI080952NIAID NIH HHS K08 AI102971NIAID NIH HHS K24 AI089794NIAID NIH HHS L30 AI091018
6 · The paper itself

Abstract

Leprosy is a chronic disease characterized by skin and peripheral nerve pathology and immune responses that fail to control Mycobacterium leprae. Toll-interacting protein (TOLLIP) regulates Toll-like receptor (TLR) and interleukin 1 receptor (IL-1R) signaling against mycobacteria. We analyzed messenger RNA (mRNA) expression of candidate immune genes in skin biopsy specimens from 85 individuals with leprosy. TOLLIP mRNA was highly and specifically correlated with IL-1R antagonist (IL-1Ra). In a case-control gene-association study with 477 cases and 1021 controls in Nepal, TOLLIP single-nucleotide polymorphism rs3793964 TT genotype was associated with increased susceptibility to leprosy (recessive, P = 1.4 × 10(-3)) and with increased skin expression of TOLLIP and IL-1Ra. Stimulation of TOLLIP-deficient monocytes with M. leprae produced significantly less IL-1Ra (P < .001), compared with control. These data suggest that M. leprae upregulates IL-1Ra by a TOLLIP-dependent mechanism. Inhibition of TOLLIP may decrease an individual's susceptibility to leprosy and offer a novel therapeutic target for IL-1-dependent diseases.

Indexed as

Genetic Predisposition to DiseasePolymorphism, Single NucleotideAdultCase-Control StudiesGene Expression Regulation, BacterialGenotypeHumansInterleukin 1 Receptor Antagonist ProteinIntracellular Signaling Peptides and ProteinsLeprosyNepalProspective StudiesSkinInterleukin 1 Receptor Antagonist ProteinIntracellular Signaling Peptides and ProteinsTOLLIP protein, humangeneticsIL-1IL-1RaIL-1 receptorimmune evasionleprosyMycobacterium lepraeSkin immunityTLR regulationTOLLIP

Identifiers

PMID26610735
PMCPMC4779304
OpenAlexW2319598394

What OpenQuestion holds

Textmetadata
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.