Evidence map›Paper›PMID 18177245›Full record

ArticleThe Journal of infectious diseases2008

Toll-like receptor 2 (TLR2) polymorphisms are associated with reversal reaction in leprosy.

Pierre-Yves Bochud, Thomas R Hawn, M Ruby Siddiqui, Paul Saunderson, Sven Britton, Isaac Abraham, Azeb Tadesse Argaw, Marta Janer, Lue Ping Zhao, Gilla Kaplan and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
8.8field-weighted citation impact, top 2% 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

63 citing papers in PubMed, 144 citations in OpenAlex.

  1. Pleiotropic effects for Parkin and LRRK2 in leprosy type-1 reactions and Parkinson's disease.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Trial
  2. Serum Neurofilament Light Chain Levels in Leprosy Patients: A Cross-Sectional Study.Tropical medicine & international health : TM & IH · 2026
    Observational
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  15. Differential Expression of IFN-Journal of immunology research · 2019
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  20. Innate Immune Responses in Leprosy.Frontiers in immunology · 2018
    Review

3 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

11 authors at 8 institutions in 5 countries.

Pierre-Yves BochudInstitute for Systems Biology, Seattle, WA 98103-8904, USA. pyb@systemsbiology.org
Thomas R Hawn
M Ruby Siddiqui
Paul Saunderson
Sven Britton
Isaac Abraham
Azeb Tadesse Argaw
Marta Janer
Lue Ping Zhao
Gilla Kaplan
Alan Aderem
Armauer Hansen Research Institute · ETCape Town HVTN Immunology Laboratory / Hutchinson Centre Research Institute of South Africa · ZAAll Africa Leprosy Tuberculosis and Rehabilitation Training Centre · ETCancer Research Center · USGenesis Research Institute · JPInstitute for Systems Biology · USInSysBio (Russia) · RUUniversity Hospital, Newark · US

Funding

Systems Approach to Innate Immunity-Inflammation-SepsisU54AI054523 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI ULEVITCH, RICHARD J · 2002 to 2006
$28.0M
LPS Signaling in Macrophages: The Roll of TollR01AI032972 · NIAID · UNIVERSITY OF WASHINGTON · PI ADEREM, ALAN A · 1992 to 2020
$14.6M
LPS REGULATION OF MACROPHAGE FUNCTIONR01AI025032 · NIAID · SEATTLE BIOMEDICAL RESEARCH INSTITUTE · PI ADEREM, ALAN A · 1987 to 2016
$6.7M
LPS REGULATION OF MACROPHAGE FUNCTIONR37AI025032 · NIAID · UNIVERSITY OF WASHINGTON · PI ADEREM, ALAN A · 1995 to 2004
$2.4M
PATHOBIOLOGY OF LEPROSYR01AI022616 · NIAID · ROCKEFELLER UNIVERSITY · PI KAPLAN, GILLA · 1989 to 2002
$1.1M
PATHOBIOLOGY OF HUMAN LEPROSYR22AI022616 · NIAID · ROCKEFELLER UNIVERSITY · PI KAPLAN, GILLA · 1986 to 1991
–
NIAID NIH HHS AI22616NIAID NIH HHS AI25032NIAID NIH HHS R01 AI025032NIAID NIH HHS R01 AI032972NIAID NIH HHS R37 AI025032NIAID NIH HHS U54 AI054523
6 · The paper itself

Abstract

backgroundLeprosy is characterized by a spectrum of clinical manifestations that depend on the type of immune response against the pathogen. Patients may undergo immunological changes known as "reactional states" (reversal reaction and erythema nodosum leprosum) that result in major clinical deterioration. The goal of the present study was to assess the effect of Toll-like receptor 2 (TLR2) polymorphisms on susceptibility to and clinical presentation of leprosy.

methodsThree polymorphisms in TLR2 (597C-->T, 1350T-->C, and a microsatellite marker) were analyzed in 431 Ethiopian patients with leprosy and 187 control subjects. The polymorphism-associated risk of developing leprosy, lepromatous (vs. tuberculoid) leprosy, and leprosy reactions was assessed by multivariate logistic regression models.

resultsThe microsatellite and the 597C-->T polymorphisms both influenced susceptibility to reversal reaction. Although the 597T allele had a protective effect (odds ratio [OR], 0.34 [95% confidence interval {CI}, 0.17-0.68]; P= .002 under the dominant model), homozygosity for the 280-bp allelic length of the microsatellite strongly increased the risk of reversal reaction (OR, 5.83 [95% CI, 1.98-17.15]; P= .001 under the recessive model). These associations were consistent among 3 different ethnic groups.

conclusionsThese data suggest a significant role for TLR-2 in the occurrence of leprosy reversal reaction and provide new insights into the immunogenetics of the disease.

Indexed as

Genetic Predisposition to DiseasePolymorphism, GeneticAdolescentAdultCase-Control StudiesChildChild, PreschoolEthiopiaFemaleHaplotypesHumansInfantInfant, NewbornLeprosyLinkage DisequilibriumMaleToll-Like Receptor 2

Identifiers

PMID18177245
PMCPMC3077295
OpenAlexW2099315201

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.