Evidence map›Paper›PMID 24067789›Full record

ArticleGenes and immunity2013

The MyD88 rs6853 and TIRAP rs8177374 polymorphic sites are associated with resistance to human pulmonary tuberculosis.

R Capparelli, F De Chiara, A Di Matteo, C Medaglia, D Iannelli

Abstract read
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In one paragraph

Article in Genes and immunity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
–field-weighted citation impact
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

13 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. The Roles of Inflammasomes in Host Defense againstPathogens (Basel, Switzerland) · 2021
    Review
  6. Article
  7. Review
  8. Review
  9. Association of theJournal of thoracic disease · 2019
    Article
  10. MyD88 in Mycobacterium tuberculosis infection.Medical microbiology and immunology · 2017
    Review
  11. Article
  12. The -938C>A Polymorphism inDisease markers · 2016
    Article
  13. 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

5 authors.

R CapparelliDepartment DiSSPAPA, University of Naples 'Federico II'
F De Chiara
A Di Matteo
C Medaglia
D Iannelli

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Toll-like receptors recognize several components of Mycobacterium tuberculosis, the main causative agent of tuberculosis. The signaling pathways leading to activation of the immune response require the MyD88 and TIRAP genes. The hypothesis that polymorphic variants of these genes influenced resistance to pulmonary tuberculosis was tested by a case-control study (400 cases and 400 controls). Heterozygosity at the polymorphic sites MyD88 rs6853 (alleles: A, G) or TIRAP rs8177374 (S180L) (alleles: C, T) is associated with resistance to pulmonary tuberculosis (P: 7.8 × 10(-8) and 2 × 10(-6), respectively). Double heterozygosity confers higher protection levels (P: 10(-14) to 2 × 10(-16)). The logistic regression model displayed that the double homozygous genotype GG/TT predisposes to the disease (odds ratio (OR): 5.78) and the AG/TT genotype combination neutralizes the protective activity exerted by AG (OR: 3.05). The same model showed that the risk of developing the disease increases with age from 31-40 years to 71-80 years (OR: 1.32-13.59).

Indexed as

Polymorphism, Single NucleotideAdultAgedAge FactorsAmino Acid SequenceCase-Control StudiesDisease ResistanceFemaleHeterozygoteHumansMaleMembrane GlycoproteinsMiddle AgedModels, GeneticMolecular Sequence DataMyeloid Differentiation Factor 88Membrane GlycoproteinsMYD88 protein, humanMyeloid Differentiation Factor 88Receptors, Interleukin-1TIRAP protein, human

Identifiers

PMID24067789

What OpenQuestion holds

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Registered trials

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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.