Evidence map›Paper›PMID 25275318›Full record

Trial reportPLoS pathogens2014

Mycobacterial antigen driven activation of CD14++CD16- monocytes is a predictor of tuberculosis-associated immune reconstitution inflammatory syndrome.

Bruno B Andrade, Amrit Singh, Gopalan Narendran, Melissa E Schechter, Kaustuv Nayak, Sudha Subramanian, Selvaraj Anbalagan, Stig M R Jensen, Brian O Porter, Lis R Antonelli and 9 more

Registry-linked trialOpen access · goldAbstract readRandomized Controlled Trial
In one paragraph

Trial report in PLoS pathogens, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02652546 (A Phase 1 Study of CC-11050 in Human Immunodeficiency Virus-1-Infected Adults With Suppressed Plasma Viremia on Antiretroviral Therapy), which is not on this map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
14.1field-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.

NCT02652546 phase1completednot on this mapstarted 2016, after this paper: background citation

A Phase 1 Study of CC-11050 in Human Immunodeficiency Virus-1-Infected Adults With Suppressed Plasma Viremia on Antiretroviral Therapy

TypeinterventionalSponsorNational Institute of Allergy and Infectious Diseases (NIAID)Ran2016 to 2018Enrolled38ConditionsHIV, InflammationArmsAssess Safety, Effect of drug on viral load, Effect of drug on T-cell count, Effect of drug on inflammatory biomarkers
3 · Its place in the literature

Who cites it

77 citing papers in PubMed, 116 citations in OpenAlex.

  1. Trial
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  4. Article
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  8. Effect of Immunomodulating Extract and Some Isolates fromMolecules (Basel, Switzerland) · 2023
    Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Phenotypic Profile ofOpen forum infectious diseases · 2023
    Article
  14. Article
  15. Frequency of CXCR3Frontiers in immunology · 2022
    Article
  16. Observational
  17. Article
  18. Article
  19. Review
  20. Article

17 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

19 authors at 6 institutions in 5 countries.

Bruno B AndradeImmunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Amrit SinghClinical and Molecular Retrovirology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Gopalan NarendranNational Institute for Research in Tuberculosis, Chennai, India.
Melissa E SchechterClinical and Molecular Retrovirology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Kaustuv NayakNational Institute for Research in Tuberculosis, Chennai, India.
Sudha SubramanianNational Institute for Research in Tuberculosis, Chennai, India.
Selvaraj AnbalaganNational Institute for Research in Tuberculosis, Chennai, India.
Stig M R JensenClinical and Molecular Retrovirology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Brian O PorterClinical and Molecular Retrovirology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Lis R AntonelliLaboratório de Imunopatologia, Centro de Pesquisas René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, Minas Gerais, Brazil.
Katalin A WilkinsonClinical Infectious Diseases Research Initiative, Institute of Infectious Disease and Molecular Medicine, and Department of Medicine, University of Cape Town, Cape Town, South Africa.
Robert J WilkinsonClinical Infectious Diseases Research Initiative, Institute of Infectious Disease and Molecular Medicine, and Department of Medicine, University of Cape Town, Cape Town, South Africa; Department of Medicine, Imperial College London, London, United Kingdom; MRC National Institute for Medical Research, London, United Kingdom.
Graeme MeintjesClinical Infectious Diseases Research Initiative, Institute of Infectious Disease and Molecular Medicine, and Department of Medicine, University of Cape Town, Cape Town, South Africa; Department of Medicine, Imperial College London, London, United Kingdom.
Helen van der PlasClinical Infectious Diseases Research Initiative, Institute of Infectious Disease and Molecular Medicine, and Department of Medicine, University of Cape Town, Cape Town, South Africa.
Dean FollmannBiostatistics Research Branch, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Daniel L BarberT-Lymphocyte Biology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Soumya SwaminathanNational Institute for Research in Tuberculosis, Chennai, India.
Alan SherImmunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
Irini SeretiClinical and Molecular Retrovirology Section, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, United States of America.
National Institute of Allergy and Infectious Diseases · USNational Institute of Research in Tuberculosis · INNational Institutes of Health · USWellcome Centre for Infectious Diseases Research in Africa · ZAFundação Oswaldo Cruz · BRImperial College London · GB

Funding

Immunopathogenic Mechanisms of Human Immunodeficiency Virus (HIV) DiseaseZIAAI001121 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SERETI, IRINI · 2010 to 2025
$27.2M
Regulation Of Immunopathology In Bacterial And Parasitic DiseaseZIAAI000843 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI SHER, ALAN · 2009 to 2022
$11.1M
Trial for the Optimal Timing of HIV Therapy after Cryptococcal MeningitisU01AI089244 · NIAID · UNIVERSITY OF MINNESOTA · PI BOULWARE, DAVID R · 2010 to 2014
$7.6M
Medical Research Council MC_U117588499Medical Research Council U1175.02.002.00014.01NIAID NIH HHS U01 AI089244NIAID NIH HHS U01AI089244Wellcome Trust 084323Wellcome Trust 088316Wellcome Trust 098316Wellcome Trust 104803
6 · The paper itself

Abstract

Paradoxical tuberculosis-associated immune reconstitution inflammatory syndrome (TB-IRIS) is an aberrant inflammatory response occurring in a subset of TB-HIV co-infected patients initiating anti-retroviral therapy (ART). Here, we examined monocyte activation by prospectively quantitating pro-inflammatory plasma markers and monocyte subsets in TB-HIV co-infected patients from a South Indian cohort at baseline and following ART initiation at the time of IRIS, or at equivalent time points in non-IRIS controls. Pro-inflammatory biomarkers of innate and myeloid cell activation were increased in plasma of IRIS patients pre-ART and at the time of IRIS; this association was confirmed in a second cohort in South Africa. Increased expression of these markers correlated with elevated antigen load as measured by higher sputum culture grade and shorter duration of anti-TB therapy. Phenotypic analysis revealed the frequency of CD14(++)CD16(-) monocytes was an independent predictor of TB-IRIS, and was closely associated with plasma levels of CRP, TNF, IL-6 and tissue factor during IRIS. In addition, production of inflammatory cytokines by monocytes was higher in IRIS patients compared to controls pre-ART. These data point to a major role of mycobacterial antigen load and myeloid cell hyperactivation in the pathogenesis of TB-IRIS, and implicate monocytes and monocyte-derived cytokines as potential targets for TB-IRIS prevention or treatment.

Indexed as

AdultAntigens, BacterialAntiretroviral Therapy, Highly ActiveBiomarkersFemaleGPI-Linked ProteinsHumansImmune Reconstitution Inflammatory SyndromeLipopolysaccharide ReceptorsMaleMonocytesReceptors, IgGTuberculosisAntigens, BacterialBiomarkersFCGR3B protein, humanGPI-Linked ProteinsLipopolysaccharide ReceptorsReceptors, IgG

Identifiers

PMID25275318
PMCPMC4183698
OpenAlexW2000074951

What OpenQuestion holds

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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.