Evidence map›Paper›PMID 20421474›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2010

Mast cells elicit proinflammatory but not type I interferon responses upon activation of TLRs by bacteria.

Nicole Dietrich, Manfred Rohde, Robert Geffers, Andrea Kröger, Hansjörg Hauser, Siegfried Weiss, Nelson O Gekara

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

38 citing papers in PubMed, 77 citations in OpenAlex.

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  16. Mast Cells in Viral, Bacterial, and Fungal Infection Immunity.International journal of molecular sciences · 2019
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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

7 authors at 3 institutions in 2 countries.

Nicole DietrichDepartment of Molecular Immunology, Helmholtz-Centre for Infection Research, 38124 Braunschweig, Germany.
Manfred Rohde
Robert Geffers
Andrea Kröger
Hansjörg Hauser
Siegfried Weiss
Nelson O Gekara
Helmholtz Centre for Infection Research · DELasell College · USMicrobial ID (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Balanced induction of proinflammatory and type I IFN responses upon activation of Toll-like receptors (TLRs) determines the outcome of microbial infections and the pathogenesis of autoimmune and other inflammatory diseases. Mast cells, key components of the innate immune system, are known for their debilitating role in allergy and autoimmunity. However, their role in antimicrobial host defenses is being acknowledged increasingly. How mast cells interact with microbes and the nature of responses triggered thereby is not well characterized. Here we show that in response to TLR activation by Gram-positive and -negative bacteria or their components, mast cells elicit proinflammatory but not type I IFN responses. We demonstrate that in mast cells, bound bacteria and TLR ligands remain trapped at the cell surface and do not undergo internalization, a prerequisite for type I IFN induction. Such cells, however, can elicit type I IFNs in response to vesicular stomatitis virus which accesses the cytosolic retinoic acid-inducible gene I receptor. Although important for antiviral immunity, a strong I IFN response is known to contribute to pathogenesis of several bacterial pathogens such as Listeria monocytogenes. Interestingly, we observed that the mast cell-dependent neutrophil mobilization upon L. monocytogenes infection is highly impaired by IFN-beta. Thus, the fact that mast cells, although endowed with the capacity to elicit type I IFNs in response to viral infection, elicit only proinflammatory responses upon bacterial infection shows that mast cells, key effector cells of the innate immune system, are well adjusted for optimal antibacterial and antiviral responses.

Indexed as

AcidsAnimalsBiological TransportCell CompartmentationCell MovementEndocytosisEndosomesGene Expression RegulationInflammation MediatorsInterferon-betaIntracellular SpaceLipopolysaccharidesListeria monocytogenesMast CellsMiceMice, Inbred BALB CAcidsInflammation MediatorsInterferon-betaLipopolysaccharidesToll-Like Receptor 4Toll-Like Receptors

Identifiers

PMID20421474
PMCPMC2889343
OpenAlexW2080181698

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.