Evidence map›Paper›PMID 30262883›Full record

Trial reportScientific reports2018

Immunological correlates of mycobacterial growth inhibition describe a spectrum of tuberculosis infection.

Matthew K O'Shea, Rachel Tanner, Julius Müller, Stephanie A Harris, Danny Wright, Lisa Stockdale, Elena Stylianou, Iman Satti, Steven G Smith, James Dunbar and 4 more

Open access · goldAbstract readClinical TrialMulticenter Study
In one paragraph

Trial report in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
4.6field-weighted citation impact, top 4% 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

27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 55 citations in OpenAlex.

  1. Pooled it
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  17. TheF1000Research · 2021
    Article
  18. Article
  19. Article
  20. The Many Hosts of Mycobacteria 8 (MHM8): A conference report.Tuberculosis (Edinburgh, Scotland) · 2020
    Review
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 6 institutions in 1 country.

Matthew K O'SheaThe Jenner Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK. m.k.oshea@bham.ac.uk.
Rachel TannerThe Jenner Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Julius MüllerThe Jenner Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK.ORCID http://orcid.org/0000-0002-1046-2968
Stephanie A HarrisThe Jenner Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Danny WrightThe Jenner Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Lisa StockdaleDepartment of Immunology and Infection, London School of Hygiene and Tropical Medicine, London, UK.
Elena StylianouThe Jenner Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Iman SattiThe Jenner Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
Steven G SmithDepartment of Immunology and Infection, London School of Hygiene and Tropical Medicine, London, UK.
James DunbarThe Friarage Hospital, Northallerton, Yorkshire, UK.
Thomas E FletcherLiverpool School of Tropical Medicine and Hygiene, Liverpool, UK.
Martin DedicoatHeartlands Hospital, Birmingham, UK.
Adam F CunninghamInstitute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK.
Helen McShaneThe Jenner Institute, Nuffield Department of Medicine, University of Oxford, Oxford, UK.
University of Oxford · GBLondon School of Hygiene & Tropical Medicine · GBFriarage Hospital · GBHeartlands Hospital · GBLiverpool School of Tropical Medicine · GBUniversity of Birmingham · GB

Funding

Wellcome TrustWellcome Trust 103420/Z/13/Z
6 · The paper itself

Abstract

A major contribution to the burden of Tuberculosis (TB) comes from latent Mycobacterium tuberculosis infections (LTBI) becoming clinically active. TB and LTBI probably exist as a spectrum and currently there are no correlates available to identify individuals with LTBI most at risk of developing active disease. We set out to identify immune parameters associated with ex vivo mycobacterial growth control among individuals with active TB disease or LTBI to define the spectrum of TB infection. We used a whole blood mycobacterial growth inhibition assay to generate a functional profile of growth control among individuals with TB, LTBI or uninfected controls. We subsequently used a multi-platform approach to identify an immune signature associated with this profile. We show, for the first time, that patients with active disease had the greatest control of mycobacterial growth, whilst there was a continuum of responses among latently infected patients, likely related to the degree of immune activation in response to bacillary load. Control correlated with multiple factors including inflammatory monocytes, activated and atypical memory B cells, IgG1 responses to TB-specific antigens and serum cytokines/chemokines. Our findings offer a method to stratify subclinical TB infections and the future potential to identify individuals most at risk of progressing to active disease and benefit from chemoprophylaxis.

Indexed as

AdultAntibodies, BacterialB-LymphocytesChemokinesFemaleHumansImmunoglobulin GLatent TuberculosisMaleMonocytesMycobacterium tuberculosisAntibodies, BacterialChemokinesImmunoglobulin G

Identifiers

PMID30262883
PMCPMC6160428
OpenAlexW2889895558

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.