Evidence map›Paper›PMID 31851971›Full record

ArticleJournal of innate immunity2020

HSV-1/TLR9-Mediated IFNβ and TNFα Induction Is Mal-Dependent in Macrophages.

Joanna Zyzak, Małgorzata Mitkiewicz, Ewa Leszczyńska, Patryk Reniewicz, Paul N Moynagh, Jakub Siednienko

Open access · goldAbstract read
In one paragraph

Article in Journal of innate immunity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

27 citing papers in PubMed, 32 citations in OpenAlex.

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  10. Recognition of Mycobacterium tuberculosis by macrophage Toll-like receptor and its role in autophagy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
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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

6 authors at 4 institutions in 2 countries.

Joanna ZyzakLaboratory of Microbiome Immunobiology, Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland.
Małgorzata MitkiewiczLaboratory of Microbiome Immunobiology, Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland.
Ewa LeszczyńskaLaboratory of Microbiome Immunobiology, Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland.
Patryk ReniewiczLaboratory of Microbiome Immunobiology, Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland.
Paul N MoynaghInstitute of Immunology, Department of Biology, Maynooth University, Maynooth, Ireland.
Jakub SiednienkoLaboratory of Microbiome Immunobiology, Ludwik Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland, jakub.siednienko@hirszfeld.pl.
Łukasiewicz Research Network – PORT Polish Center for Technology Development · PLLudwik Hirszfeld Institute of Immunology and Experimental Therapy · PLNational University of Ireland, Maynooth · IEPolish Academy of Sciences · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Innate immune response is a universal mechanism against invading pathogens. Toll-like receptors (TLRs), being part of a first line of defense, are responsible for detecting a variety of microorganisms. Among them TLR9, which is localized in endosomes, acts as a sensor for unmethylated CpG motifs present in bacteria, DNA viruses (e.g., HSV-1), or fungi. TLRs differ from one another by the use of accessory proteins. MyD88 adapter-like (Mal) adapter molecule is considered a positive regulator of TLR2- and TLR4-dependent pathways. It has been reported that this adapter may also negatively control signal transduction induced by TLR3 anchored in the endosome membrane. So far, the role of Mal adapter protein in the TLR9 signaling pathways has not been clarified. We show for the first time that Mal is engaged in TLR9-de-pendent expression of genes encoding IFNβ and TNFα in HSV-1-infected or CpG-C-treated macrophages and requires a noncanonical NF-κB pathway. Moreover, using inhibitor of ERK1/2 we confirmed involvement of these kinases in TLR9-dependent induction of IFNβ and TNFα. Our study points to a new role of Mal in TLR9 signaling through a hitherto unknown mechanism whereby lack of Mal specifically impairs ERK1/2-mediated induction of noncanonical NF-κB pathway and concomitant IFNβ and TNFα production.

Indexed as

AnimalsHerpesvirus 1, HumanHumansInterferon-betaMacrophagesMembrane GlycoproteinsMiceMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NF-kappa BPhosphorylationReceptors, Interleukin-1Signal TransductionToll-Like Receptor 9Tumor Necrosis Factor-alphaInterferon-betaMembrane GlycoproteinsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NF-kappa BReceptors, Interleukin-1TIRAP protein, mouseToll-Like Receptor 9Tumor Necrosis Factor-alphaHSV-1IFNβMal/TIRAPNF-κBToll-like receptor 9

Identifiers

PMID31851971
PMCPMC7506264
OpenAlexW2996156649

What OpenQuestion holds

Textmetadata
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.