Evidence map›Paper›PMID 25369333›Full record

ArticlePloS one2014

CD161+ MAIT cells are severely reduced in peripheral blood and lymph nodes of HIV-infected individuals independently of disease progression.

Johanna Maria Eberhard, Philip Hartjen, Silke Kummer, Reinhold E Schmidt, Maximilian Bockhorn, Clara Lehmann, Ashwin Balagopal, Joachim Hauber, Jan van Lunzen, Julian Schulze zur Wiesch

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

46 citing papers in PubMed, 67 citations in OpenAlex.

  1. Gastrointestinal MAIT cells in chronic HIV-1 infection.Journal of immunology (Baltimore, Md. : 1950) · 2026
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  10. The Emerging Role of MAIT Cell Responses in Viral Infections.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Review
  11. MAIT cells and the microbiome.Frontiers in immunology · 2023
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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

10 authors at 5 institutions in 2 countries.

Johanna Maria EberhardInfectious Diseases Unit, Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Heinrich Pette Institute - Leibniz Institute for Experimental Virology, Hamburg, Germany.
Philip HartjenInfectious Diseases Unit, Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Department of Oral and Maxillofacial Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Heinrich Pette Institute - Leibniz Institute for Experimental Virology, Hamburg, Germany.
Silke KummerInfectious Diseases Unit, Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Heinrich Pette Institute - Leibniz Institute for Experimental Virology, Hamburg, Germany.
Reinhold E SchmidtDepartment of Immunology and Rheumatology, Hannover Medical School, Hanover, Germany; German Center for Infection Research (DZIF), partner site Hamburg and Hannover, Hamburg and Hannover, Germany.
Maximilian BockhornDepartment of General Surgery, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Clara LehmannDepartment of Internal Medicine I, University Hospital of Cologne, Cologne, Germany.
Ashwin BalagopalSchool of Medicine, Johns Hopkins University, Baltimore, Maryland, United States of America.
Joachim HauberHeinrich Pette Institute - Leibniz Institute for Experimental Virology, Hamburg, Germany; German Center for Infection Research (DZIF), partner site Hamburg and Hannover, Hamburg and Hannover, Germany.
Jan van LunzenInfectious Diseases Unit, Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Heinrich Pette Institute - Leibniz Institute for Experimental Virology, Hamburg, Germany; German Center for Infection Research (DZIF), partner site Hamburg and Hannover, Hamburg and Hannover, Germany.
Julian Schulze zur WieschInfectious Diseases Unit, Department of Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany; Heinrich Pette Institute - Leibniz Institute for Experimental Virology, Hamburg, Germany; German Center for Infection Research (DZIF), partner site Hamburg and Hannover, Hamburg and Hannover, Germany.
German Center for Infection Research · DEUniversität Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DEJohns Hopkins Medicine · USUniversity Hospital Cologne · DE

Funding

The Progression of Hepatitis C Among IDUs with HIVR01DA016078 · NIDA · JOHNS HOPKINS UNIVERSITY · PI BALAGOPAL, ASHWIN, THOMAS, DAVID L · 2002 to 2016
$10.9M
NIDA NIH HHS R01 DA016078
6 · The paper itself

Abstract

Mucosal-associated invariant T (MAIT) cells are characterized by the combined expression of the semi-invariant T cell receptor (TCR) Vα7.2, the lectin receptor CD161, as well as IL-18R, and play an important role in antibacterial host defense of the gut. The current study characterized CD161(+) MAIT and CD161-TCRVα7.2(+) T cell subsets within a large cohort of HIV patients with emphasis on patients with slow disease progression and elite controllers. Mononuclear cells from blood and lymph node samples as well as plasma from 63 patients and 26 healthy donors were analyzed by multicolor flow cytometry and ELISA for IL-18, sCD14 and sCD163. Additionally, MAIT cells were analyzed after in vitro stimulation with different cytokines and/or fixed E.coli. Reduced numbers of CD161(+) MAIT cells during HIV infection were detectable in the blood and lymph nodes of all patient groups, including elite controllers. CD161+ MAIT cell numbers did not recover even after successful antiretroviral treatment. The loss of CD161(+) MAIT cells was correlated with higher levels of MAIT cell activation; an increased frequency of the CD161-TCRVα7.2(+)T cell subset in HIV infection was observed. In vitro stimulation of MAIT cells with IL-18 and IL-12, IL-7 and fixed E.coli also resulted in a rapid and additive reduction of the MAIT cell frequency defined by CD161, IL-18R and CCR6. In summary, the irreversible reduction of the CD161(+) MAIT cell subset seems to be an early event in HIV infection that is independent of later stages of the disease. This loss appears to be at least partially due to the distinctive vulnerability of MAIT cells to the pronounced stimulation by microbial products and cytokines during HIV-infection.

Indexed as

AdultAgedAntigens, CDAntigens, Differentiation, MyelomonocyticAnti-HIV AgentsCD163 AntigenDisease ProgressionEscherichia coliFemaleHIV InfectionsHumansImmunity, MucosalInterleukin-12Interleukin-18Interleukin-7Leukocytes, MononuclearAntigens, CDAntigens, Differentiation, MyelomonocyticAnti-HIV AgentsCD163 AntigenInterleukin-12Interleukin-18Interleukin-7Lipopolysaccharide ReceptorsNK Cell Lectin-Like Receptor Subfamily BReceptors, Antigen, T-Cell, alpha-betaReceptors, Cell SurfaceReceptors, Interleukin-18

Identifiers

PMID25369333
PMCPMC4219715
OpenAlexW1972989279

What OpenQuestion holds

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Registered trials

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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.