Evidence map›Paper›PMID 14735149›Full record

ArticleGenes and immunity2004

Evidence for a cluster of genes on chromosome 17q11-q21 controlling susceptibility to tuberculosis and leprosy in Brazilians.

S E Jamieson, E N Miller, G F Black, C S Peacock, H J Cordell, J M M Howson, M-A Shaw, D Burgner, W Xu, Z Lins-Lainson and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Genes and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed, 3 pooled it
3.4field-weighted citation impact, top 7% 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

68 citing papers in PubMed, 3 syntheses or guidelines pooled it, 146 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Lewis Y (LeImmunologic research · 2026
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Genetics and evolution of tuberculosis pathogenesis: New perspectives and approaches.Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases · 2020
    Review
  10. Article
  11. The Research Progress of Host Genes and Tuberculosis Susceptibility.Oxidative medicine and cellular longevity · 2019
    Review
  12. Review
  13. Article
  14. Susceptibility toFrontiers in microbiology · 2017
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

8 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

14 authors at 7 institutions in 2 countries.

S E JamiesonCambridge Institute for Medical Research, University of Cambridge School of Clinical Medicine, Addenbrookes Hospital, Cambridge, UK.
E N Miller
G F Black
C S Peacock
H J Cordell
J M M Howson
M-A Shaw
D Burgner
W Xu
Z Lins-Lainson
J J Shaw
F Ramos
F Silveira
J M Blackwell
Addenbrooke's Hospital · GBInstituto Evandro Chagas · BRCentre for Human Genetics · GBUniversidade de São Paulo · BRUniversity College London · GBUniversity of Cambridge · GBUniversity of Leeds · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The region of conserved synteny on mouse chromosome 11/human 17q11-q21 is known to carry a susceptibility gene(s) for intramacrophage pathogens. The region is rich in candidates including NOS2A, CCL2/MCP-1, CCL3/MIP-1alpha, CCL4/MIP-1beta, CCL5/RANTES, CCR7, STAT3 and STAT5A/5B. To examine the region in man, we studied 92 multicase tuberculosis (627 individuals) and 72 multicase leprosy (372 individuals) families from Brazil. Multipoint nonparametric analysis (ALLEGRO) using 16 microsatellites shows two peaks of linkage for leprosy at D17S250 (Z(lr) score 2.34; P=0.01) and D17S1795 (Z(lr) 2.67; P=0.004) and a single peak for tuberculosis at D17S250 (Z(lr) 2.04; P=0.02). Combined analysis shows significant linkage (peak Z(lr) 3.38) at D17S250, equivalent to an allele sharing LOD score 2.48 (P=0.0004). To determine whether one or multiple genes contribute, 49 informative single nucleotide polymorphisms were typed in candidate genes. Family-based allelic association testing that was robust to family clustering demonstrated significant associations with tuberculosis susceptibility at four loci separated by intervals (NOS2A-8.4 Mb-CCL18-32.3 kb-CCL4-6.04 Mb-STAT5B) up to several Mb. Stepwise conditional logistic regression analysis using a case/pseudo-control data set showed that the four genes contributed separate main effects, consistent with a cluster of susceptibility genes across 17q11.2.

Indexed as

Genetic Predisposition to DiseaseMilk ProteinsAnimalsBrazilCase-Control StudiesChemokine CCL3Chemokine CCL4Chemokines, CCChromosomes, Human, Pair 17DNA-Binding ProteinsFemaleGene FrequencyGenetic MarkersGenetic TestingGenotypeHumansCCL18 protein, humanCCL4 protein, humanChemokine CCL3Chemokine CCL4Chemokines, CCDNA-Binding ProteinsGenetic MarkersMacrophage Inflammatory ProteinsMilk ProteinsProteinsSTAT5A protein, humanStat5a protein, mouseSTAT5B protein, humanStat5b protein, mouseSTAT5 Transcription FactorTrans-ActivatorsTumor Suppressor Proteins

Identifiers

PMID14735149
OpenAlexW2088946841

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.