Evidence map›Paper›PMID 25143364›Full record

ArticleScience translational medicine2014

IL-32 is a molecular marker of a host defense network in human tuberculosis.

Dennis Montoya, Megan S Inkeles, Phillip T Liu, Susan Realegeno, Rosane M B Teles, Poorva Vaidya, Marcos A Munoz, Mirjam Schenk, William R Swindell, Rene Chun and 7 more

Abstract read
In one paragraph

Article in Science translational medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

63 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. microLife · 2023
    Article
  10. Article
  11. Review
  12. Article
  13. Lipophosphoglycan From Dermotropic New WorldFrontiers in cellular and infection microbiology · 2022
    Article
  14. Article
  15. Article
  16. Genetics and Functional Mechanisms of STAT3 Polymorphisms in Human Tuberculosis.Frontiers in cellular and infection microbiology · 2021
    Article
  17. Article
  18. Review
  19. Review
  20. Article

3 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

17 authors at 3 institutions in 1 country.

Dennis MontoyaDivision of Dermatology, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA 90095, USA.
Megan S InkelesDepartment of Molecular, Cell, and Developmental Biology, UCLA, Los Angeles, CA 90095, USA.
Phillip T LiuDivision of Dermatology, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA 90095, USA. UCLA/Orthopaedic Hospital, Department of Orthopaedic Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Susan RealegenoDivision of Dermatology, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA 90095, USA. Department of Microbiology, Immunology and Molecular Genetics, UCLA, Los Angeles, CA 90095 USA.
Rosane M B TelesDivision of Dermatology, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA 90095, USA.
Poorva VaidyaDivision of Dermatology, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA 90095, USA.
Marcos A MunozDivision of Dermatology, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA 90095, USA.
Mirjam SchenkDivision of Dermatology, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA 90095, USA.
William R SwindellDepartment of Dermatology, University of Michigan School of Medicine, Ann Arbor, MI 48109, USA.
Rene ChunUCLA/Orthopaedic Hospital, Department of Orthopaedic Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Kathryn ZavalaUCLA/Orthopaedic Hospital, Department of Orthopaedic Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Martin HewisonUCLA/Orthopaedic Hospital, Department of Orthopaedic Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
John S AdamsUCLA/Orthopaedic Hospital, Department of Orthopaedic Surgery, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA.
Steve HorvathHuman Genetics, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095, USA. Biostatistics, School of Public Health, UCLA, Los Angeles, CA 90095, USA.
Matteo PellegriniDepartment of Molecular, Cell, and Developmental Biology, UCLA, Los Angeles, CA 90095, USA.
Barry R BloomHarvard School of Public Health, Boston, MA 02115, USA.
Robert L ModlinDivision of Dermatology, David Geffen School of Medicine at University of California Los Angeles (UCLA), Los Angeles, CA 90095, USA. Department of Microbiology, Immunology and Molecular Genetics, UCLA, Los Angeles, CA 90095 USA. rmodlin@mednet.ucla.edu.
University of California, Los Angeles · USHarvard University · USUniversity of Michigan–Ann Arbor · US

Funding

UCLA-Caltech Medical Scientist Training ProgramT32GM008042 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI AJIJOLA, OLUJIMI A, DAWSON, DAVID WAYNE · 1985 to 2023
$29.9M
UCLA NIGMS T32 Program AssessmentT32GM007185 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI TORRES, JORGE · 1985 to 2020
$21.7M
Molecular Analysis of the Host Immune Response in LeprosyR01AI022553 · NIAID · UNIVERSITY OF SOUTHERN CALIFORNIA · PI ROBERT L MODLIN · 1989 to 2026
$15.7M
UCLA MSD ProgramR25GM055052 · NIGMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BARBER, PAUL HENRY, HASSON, TAMA W. · 1996 to 2021
$9.2M
Vitamin D Metabolism in LeprosyP50AR063020 · NIAMS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MODLIN, ROBERT L · 2012 to 2016
$7.8M
Divergence of Phagocytic and Antimicrobial Programs in LeprosyR01AI047868 · NIAID · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI MODLIN, ROBERT L · 2010 to 2014
$2.4M
Role of Vitamin D Prohormone 25-OHD in the Immune Response to TuberculosisR01HL119068 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LIU, PHILIP T., MODLIN, ROBERT L · 2014 to 2017
$1.5M
NHLBI NIH HHS R01 HL119068NIAID NIH HHS R01 AI022553NIAID NIH HHS R01AI022553NIAID NIH HHS R01 AI047868NIAMS NIH HHS P50 AR063020NIGMS NIH HHS R25 GM055052NIGMS NIH HHS T32 GM007185NIGMS NIH HHS T32 GM008042
6 · The paper itself

Abstract

Tuberculosis is a leading cause of infectious disease-related death worldwide; however, only 10% of people infected with Mycobacterium tuberculosis develop disease. Factors that contribute to protection could prove to be promising targets for M. tuberculosis therapies. Analysis of peripheral blood gene expression profiles of active tuberculosis patients has identified correlates of risk for disease or pathogenesis. We sought to identify potential human candidate markers of host defense by studying gene expression profiles of macrophages, cells that, upon infection by M. tuberculosis, can mount an antimicrobial response. Weighted gene coexpression network analysis revealed an association between the cytokine interleukin-32 (IL-32) and the vitamin D antimicrobial pathway in a network of interferon-γ- and IL-15-induced "defense response" genes. IL-32 induced the vitamin D-dependent antimicrobial peptides cathelicidin and DEFB4 and to generate antimicrobial activity in vitro, dependent on the presence of adequate 25-hydroxyvitamin D. In addition, the IL-15-induced defense response macrophage gene network was integrated with ranked pairwise comparisons of gene expression from five different clinical data sets of latent compared with active tuberculosis or healthy controls and a coexpression network derived from gene expression in patients with tuberculosis undergoing chemotherapy. Together, these analyses identified eight common genes, including IL-32, as molecular markers of latent tuberculosis and the IL-15-induced gene network. As maintaining M. tuberculosis in a latent state and preventing transition to active disease may represent a form of host resistance, these results identify IL-32 as one functional marker and potential correlate of protection against active tuberculosis.

Indexed as

Antimicrobial Cationic PeptidesBiomarkersCell DifferentiationGene Expression ProfilingHumansInterferon-gammaInterleukin-15InterleukinsMacrophagesMycobacterium tuberculosisTuberculosisVitamin DAntimicrobial Cationic PeptidesBiomarkersIL32 protein, humanInterferon-gammaInterleukin-15InterleukinsVitamin D

Identifiers

PMID25143364
PMCPMC4175914
OpenAlexW2106343561

What OpenQuestion holds

Textmetadata
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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.