Evidence map›Paper›PMID 34469846›Full record

ArticleCellular immunology2021

Evaluation of autophagy mediators in myeloid-derived suppressor cells during human tuberculosis.

Leigh A Kotze, Vinzeigh N Leukes, Zhuo Fang, Manfred B Lutz, Bryna L Fitzgerald, John Belisle, Andre G Loxton, Gerhard Walzl, Nelita du Plessis

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Review
  3. Functional Analysis of Genes inIndian journal of microbiology · 2024
    Review
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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

9 authors at 4 institutions in 3 countries.

Leigh A KotzeDSI-NRF Centre of Excellence for Biomedical Tuberculosis Research, South African Medical Research Council for Tuberculosis Research, Division of Molecular Biology and Human Genetics, Faculty of Medical and Health Sciences, Stellenbosch University, Cape Town, South Africa.
Vinzeigh N LeukesDSI-NRF Centre of Excellence for Biomedical Tuberculosis Research, South African Medical Research Council for Tuberculosis Research, Division of Molecular Biology and Human Genetics, Faculty of Medical and Health Sciences, Stellenbosch University, Cape Town, South Africa.
Zhuo FangDSI-NRF Centre of Excellence for Biomedical Tuberculosis Research, South African Medical Research Council for Tuberculosis Research, Division of Molecular Biology and Human Genetics, Faculty of Medical and Health Sciences, Stellenbosch University, Cape Town, South Africa.
Manfred B LutzInstitute of Virology and Immunobiology, University of Würzburg, Würzburg, Germany.
Bryna L FitzgeraldDepartment of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, USA.
John BelisleDepartment of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, USA.
Andre G LoxtonDSI-NRF Centre of Excellence for Biomedical Tuberculosis Research, South African Medical Research Council for Tuberculosis Research, Division of Molecular Biology and Human Genetics, Faculty of Medical and Health Sciences, Stellenbosch University, Cape Town, South Africa.
Gerhard WalzlDSI-NRF Centre of Excellence for Biomedical Tuberculosis Research, South African Medical Research Council for Tuberculosis Research, Division of Molecular Biology and Human Genetics, Faculty of Medical and Health Sciences, Stellenbosch University, Cape Town, South Africa.
Nelita du PlessisDSI-NRF Centre of Excellence for Biomedical Tuberculosis Research, South African Medical Research Council for Tuberculosis Research, Division of Molecular Biology and Human Genetics, Faculty of Medical and Health Sciences, Stellenbosch University, Cape Town, South Africa. Electronic address: nelita@sun.ac.za.
Stellenbosch University · ZAColorado State University · USSouth African Medical Research Council · ZAUniversity of Würzburg · DE

Funding

Biology and Biosignatures of Anti-Tuberculosis Treatment ResponseU01AI115619 · NIAID · COLORADO STATE UNIVERSITY · PI BELISLE, JOHN T · 2015 to 2019
$3.1M
NIAID NIH HHS U01 AI115619
6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSC) are induced during active TB disease to restore immune homeostasis but instead exacerbate disease outcome due to chronic inflammation. Autophagy, in conventional phagocytes, ensures successful clearance of M.tb. However, autophagy has been demonstrated to induce prolonged MDSC survival. Here we investigate the relationship between autophagy mediators and MDSC in the context of active TB disease and during anti-TB therapy. We demonstrate a significant increase in MDSC frequencies in untreated active TB cases with these MDSC expressing TLR4 and significantly more mTOR and IL-6 than healthy controls, with mTOR levels decreasing during anti-TB therapy. Finally, we show that HMGB1 serum concentrations decrease in parallel with mTOR. These findings suggest a complex interplay between MDSC and autophagic mediators, potentially dependent on cellular localisation and M.tb infection state.

Indexed as

Antitubercular AgentsAutophagyHMGB1 ProteinHumansInterleukin-6Myeloid-Derived Suppressor CellsTOR Serine-Threonine KinasesTuberculosisAntitubercular AgentsHMGB1 ProteinHMGB1 protein, humanIL6 protein, humanInterleukin-6MTOR protein, humanTOR Serine-Threonine KinasesAutophagyHigh mobility group box protein 1Mycobacterium tuberculosisMyeloid-derived suppressor cellsTuberculosis

Identifiers

PMID34469846
PMCPMC9278564
OpenAlexW3194893919

What OpenQuestion holds

Textmetadata
LicenceTDM
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.