Evidence map›Paper›PMID 10377182›Full record

ArticleThe Journal of experimental medicine1999

Influence of polymorphism in the genes for the interleukin (IL)-1 receptor antagonist and IL-1beta on tuberculosis.

R J Wilkinson, P Patel, M Llewelyn, C S Hirsch, G Pasvol, G Snounou, R N Davidson, Z Toossi

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 2 pooled it
11.0field-weighted citation impact, top 1% 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

82 citing papers in PubMed, 2 syntheses or guidelines pooled it, 294 citations in OpenAlex.

  1. Pooled it
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  14. Immunology ofMicrobiology spectrum · 2019
    Review
  15. Observational
  16. Patients with type 1 diabetes mellitus have impaired IL-1β production in response to Mycobacterium tuberculosis.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2018
    Article
  17. Article
  18. IL-1RN and IL-1Mediators of inflammation · 2018
    Article
  19. Article
  20. Article

22 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

8 authors at 2 institutions in 2 countries.

R J WilkinsonDivision of Infectious Diseases, Case Western Reserve University, Cleveland, Ohio 44106-4984, USA.
P Patel
M Llewelyn
C S Hirsch
G Pasvol
G Snounou
R N Davidson
Z Toossi
Case Western Reserve University · USNorthwick Park Hospital · GB

Funding

IMMUNOSUPPRESSION IN MYCOBACTERIAL DISEASESR01AI018471 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI TOOSSI, ZAHRA · 1987 to 2001
$545k
IMMUNOSUPPRESSION IN MYCOBACTERIAL DISEASESR22AI018471 · NIAID · CASE WESTERN RESERVE UNIVERSITY · PI ELLNER, JERROLD J. · 1985 to 1985
–
NIAID NIH HHS AI-18471
6 · The paper itself

Abstract

Several lines of evidence suggest that host genetic factors controlling the immune response influence infection by Mycobacterium tuberculosis. The proinflammatory cytokine interleukin (IL)-1beta and its antagonist, IL-1Ra (IL-1 receptor agonist), are strongly induced by M. tuberculosis and are encoded by polymorphic genes. The induction of both IL-1Ra mRNA and secreted protein by M. tuberculosis in IL-1Ra allele A2-positive (IL-1Ra A2(+)) healthy subjects was 1.9-fold higher than in IL-1Ra A2(-) subjects. The M. tuberculosis-induced expression of mRNA for IL-1beta was higher in subjects of the IL-1beta (+3953) A1(+) haplotype (P = 0.04). The molar ratio of IL-1Ra/IL-1beta induced by M. tuberculosis was markedly higher in IL-1Ra A2(+) individuals (P < 0.05), with minor overlap between the groups, reflecting linkage between the IL-1Ra A2 and IL-1beta (+3953) A2 alleles. In M. tuberculosis-stimulated peripheral blood mononuclear cells, the addition of IL-4 increased IL-1Ra secretion, whereas interferon gamma increased and IL-10 decreased IL-1beta production, indicative of a differential influence on the IL-1Ra/IL-1beta ratio by cytokines. In a study of 114 healthy purified protein derivative-reactive subjects and 89 patients with tuberculosis, the frequency of allelic variants at two positions (-511 and +3953) in the IL-1beta and IL-1Ra genes did not differ between the groups. However, the proinflammatory IL-1Ra A2(-)/IL-1beta (+3953) A1(+) haplotype was unevenly distributed, being more common in patients with tuberculous pleurisy (92%) in comparison with healthy M. tuberculosis-sensitized control subjects or patients with other disease forms (57%, P = 0.028 and 56%, P = 0. 024, respectively). Furthermore, the IL-1Ra A2(+) haplotype was associated with a reduced Mantoux response to purified protein derivative of M. tuberculosis: 60% of tuberculin-nonreactive patients were of this type. Thus, the polymorphism at the IL-1 locus influences the cytokine response and may be a determinant of delayed-type hypersensitivity and disease expression in human tuberculosis.

Indexed as

Polymorphism, GeneticCell DivisionGenotypeHaplotypesHumansHypersensitivity, DelayedInterleukin-1Interleukin-10Interleukin 1 Receptor Antagonist ProteinInterleukin-4Interleukin-6LeukocytesMycobacterium tuberculosisReceptors, Interleukin-1RNA, MessengerSialoglycoproteinsIL1RN protein, humanInterleukin-1Interleukin-10Interleukin 1 Receptor Antagonist ProteinInterleukin-4Interleukin-6Receptors, Interleukin-1RNA, MessengerSialoglycoproteinsTuberculin

Identifiers

PMID10377182
PMCPMC2192963
OpenAlexW2156995597

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.