ArticlePloS one2007
Full-exon resequencing reveals toll-like receptor variants contribute to human susceptibility to tuberculosis disease.
Article in PloS one, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers, 7 of them syntheses that pooled it.
What it found
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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.
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.
Who cites it
96 citing papers in PubMed, 7 syntheses or guidelines pooled it, 193 citations in OpenAlex.
- Association between interleukin-12 +1188A/C polymorphism and the risk of tuberculosis: A meta-analysis.African health sciences · 2023Pooled it
- TLR2 Arg753Gln Gene Polymorphism Associated with Tuberculosis Susceptibility: An Updated Meta-Analysis.BioMed research international · 2019Pooled it
- Association of polymorphisms in Toll-like receptors 4 and 9 with risk of pulmonary tuberculosis: a meta-analysis.Medical science monitor : international medical journal of experimental and clinical research · 2015Pooled it
- Toll-like receptor polymorphisms and tuberculosis susceptibility: A comprehensive meta-analysis.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2015Pooled it
- TLR1, 2, 4, 6 and 9 Variants Associated with Tuberculosis Susceptibility: A Systematic Review and Meta-Analysis.PloS one · 2015Pooled it
- Meta-analysis on the associations of TLR2 gene polymorphisms with pulmonary tuberculosis susceptibility among Asian populations.PloS one · 2013Pooled it
- Toll-like receptor -1, -2, and -6 polymorphisms and pulmonary tuberculosis susceptibility: a systematic review and meta-analysis.PloS one · 2013Pooled it
- Polymorphisms in Toll-Like Receptor 10 and Tuberculosis Susceptibility: Evidence from Three Independent Series.Frontiers in immunology · 2018Trial
- Genetic variation in the prostaglandin E2 pathway is associated with primary graft dysfunction.American journal of respiratory and critical care medicine · 2014Trial
- A novel expectation-maximization approach to infer general diploid selection from time-series genetic data.PLoS genetics · 2025Article
- A novel expectation-maximization approach to infer general diploid selection from time-series genetic data.bioRxiv : the preprint server for biology · 2025Article
- Innate Immunity Toll-Like Triad TLR6-1-10 and Its Diversity in Distinct Horse Breeds.Veterinary medicine and science · 2025Article
- Twelve toll-like receptor (TLR) genes in the family Equidae - comparative genomics, selection and evolution.Veterinary research communications · 2024Article
- Toll-like receptor 6 inhibits colorectal cancer progression by suppressing NF-κB signaling.Heliyon · 2024Article
- Association of Toll-like Receptors 1, 2, 4, 6, 8, 9 and 10 Genes Polymorphisms and Susceptibility to Pulmonary Tuberculosis in Sudanese Patients.ImmunoTargets and therapy · 2023Article
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- Association of Single Nucleotide Polymorphisms from Angiogenesis-Related Genes,Current issues in molecular biology · 2022Article
- Tuberculosis and Autoimmunity.Pathophysiology : the official journal of the International Society for Pathophysiology · 2022Review
- Relationship between tool-like receptor 4 gene polymorphism and the susceptibility to pulmonary tuberculosis.American journal of translational research · 2022Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Tuberculosis (TB) is the leading cause of death worldwide due to an infectious agent. Data have accumulated over decades suggesting that variability in human susceptibility to TB disease has a genetic component. Toll-like receptors (TLRs) play a critical role in initiating the innate immune response to many pathogens in mouse models, but little is known about their role in human infections. Human TLRs have been reported to recognize mycobacterial antigens and initiate an immune response. We tested the hypothesis that amino acid-altering polymorphisms in five TLRs were associated with susceptibility to TB disease using a population-based case-control study with 1,312 adult TB patients and controls. Full-coding region sequencing of the five TLR genes in all 1,312 subjects yielded a data set in excess of 16 Mb. Rare nonsynonymous polymorphisms in TLR6-TLR1-TLR10 were significantly overrepresented among African-American TB cases compared with ethnically-matched control subjects. Common nonsynonymous polymorphisms in TLR6-TLR1-TLR10 also were significantly associated with TB disease in certain ethnic groups. Among African Americans, homozygotes for the common-variant haplotype TLR1-248S, TLR1-602I, and TLR6-249S had a significantly increased TB disease risk. A transmission/disequilibrium test on an independent sample found that the TLR1-248S variant was preferentially transmitted to diseased children, thereby confirming disease association. These results are consistent with recent reports implicating TLR1 variants, including TLR1-602, in significantly altered innate immune responses. Also consistent with disease association, rare TLR6 variants were defective in their ability to mediate NF-kappaB signal transduction in transfected human cells. Taken together, the data suggest that variant TLRs contribute to human susceptibility to TB disease. Extensive full-exon resequencing was critical for revealing new information about the role of TLRs in human-pathogen interactions and the genetic basis of innate immune function.
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Registered trials
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.