Evidence map›Paper›PMID 30695101›Full record

ArticleImmunology and cell biology2019

Antibody opsonization enhances MAIT cell responsiveness to bacteria via a TNF-dependent mechanism.

Zoltán Bánki, Lisette Krabbendam, Dominik Klaver, Tianqi Leng, Simon Kruis, Hema Mehta, Brigitte Müllauer, Dorothea Orth-Höller, Heribert Stoiber, Christian B Willberg and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Immunology and cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. MAIT cells modulating the oral lichen planus immune microenvironment: a cellular crosstalk perspective.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. MAIT Cell Activation and Functions.Frontiers in immunology · 2020
    Review
  11. Mucosal-Associated Invariant T cell in liver diseases.International journal of biological sciences · 2020
    Review
  12. Article
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

11 authors at 2 institutions in 2 countries.

Zoltán BánkiDivision of Virology, Medical University of Innsbruck, Innsbruck, Austria.ORCID 0000-0002-3826-5800
Lisette KrabbendamPeter Medawar Building for Pathogen Research, University of Oxford, Oxford, UK.
Dominik KlaverDivision of Virology, Medical University of Innsbruck, Innsbruck, Austria.
Tianqi LengPeter Medawar Building for Pathogen Research, University of Oxford, Oxford, UK.
Simon KruisDivision of Virology, Medical University of Innsbruck, Innsbruck, Austria.
Hema MehtaPeter Medawar Building for Pathogen Research, University of Oxford, Oxford, UK.
Brigitte MüllauerDivision of Virology, Medical University of Innsbruck, Innsbruck, Austria.
Dorothea Orth-HöllerDivision of Hygiene and Medical Microbiology, Medical University of Innsbruck, Innsbruck, Austria.
Heribert StoiberDivision of Virology, Medical University of Innsbruck, Innsbruck, Austria.
Christian B WillbergPeter Medawar Building for Pathogen Research, University of Oxford, Oxford, UK.
Paul KlenermanPeter Medawar Building for Pathogen Research, University of Oxford, Oxford, UK.ORCID 0000-0003-4307-9161
Innsbruck Medical University · ATUniversity of Oxford · GB

Funding

Department of HealthWellcome Trust 109965/Z/15/ZWellcome Trust WT109965MA
6 · The paper itself

Abstract

Mucosal-associated invariant T (MAIT) cells are an abundant human T-cell subset with antimicrobial properties. They can respond to bacteria presented via antigen-presenting cells (APCs) such as macrophages, which present bacterially derived ligands from the riboflavin synthesis pathway on MR1. Moreover, MAIT cells are also highly responsive to cytokines which enhance and even substitute for T-cell receptor-mediated signaling. The mechanisms leading to an efficient presentation of bacteria to MAIT cells by APCs have not been fully elucidated. Here, we showed that the monocytic cell line THP-1 and B cells activated MAIT cells differentially in response to Escherichia coli. THP-1 cells were generally more potent in inducing IFNγ and IFNγ/TNF production by MAIT cells. Furthermore, THP-1, but not B, cells produced TNF upon bacterial stimulation, which in turn supported IFNγ production by MAIT cells. Finally, we addressed the role of antibody-dependent opsonization of bacteria in the activation of MAIT cells using in vitro models. We found that opsonization had a substantial impact on downstream MAIT cell activation by monocytes. This was associated with enhanced activation of monocytes and increased TNF release. Importantly, this TNF acted in concert with other cytokines to drive MAIT cell activation. These data indicate both a significant interaction between adaptive and innate immunity in the response to bacteria, and an important role for TNF in MAIT cell triggering.

Indexed as

Adaptive ImmunityAntibodies, BacterialAntigen PresentationB-LymphocytesEscherichia coliEscherichia coli InfectionsHumansImmunity, InnateInterferon-gammaLymphocyte ActivationMonocytesMucosal-Associated Invariant T CellsOpsonin ProteinsPhagocytosisSignal TransductionTHP-1 CellsAntibodies, BacterialInterferon-gammaOpsonin ProteinsTumor Necrosis Factor-alphaBacteriaE. coliIgG-opsonizationinnate T cellsMAIT cellsTNF

Identifiers

PMID30695101
PMCPMC6767153
OpenAlexW2913076663

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.