Evidence map›Paper›PMID 28421072›Full record

ArticleFrontiers in immunology2017

Dysregulated IL-1β Secretion in Autoinflammatory Diseases: A Matter of Stress?

Sonia Carta, Claudia Semino, Roberto Sitia, Anna Rubartelli

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  8. Expression and Function of Host Defense Peptides at Inflammation Sites.International journal of molecular sciences · 2019
    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

4 authors at 3 institutions in 1 country.

Sonia CartaCell Biology Unit, IRCCS AOU San Martino-IST, Genova, Italy.
Claudia SeminoUnit of Protein Transport and Secretion, Division of Genetics and Cell Biology, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Roberto SitiaUnit of Protein Transport and Secretion, Division of Genetics and Cell Biology, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Anna RubartelliCell Biology Unit, IRCCS AOU San Martino-IST, Genova, Italy.
Ospedale Policlinico San Martino · ITIstituto di Ricovero e Cura a Carattere Scientifico San RaffaeleVita-Salute San Raffaele University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Infectious and sterile inflammation is induced by activation of innate immune cells. Triggering of toll-like receptors by pathogen-associated molecular pattern or damage-associated molecular pattern (PAMP or DAMP) molecules generates reactive oxygen species that in turn induce production and activation of pro-inflammatory cytokines such as IL-1β. Recent evidence indicates that cell stress due to common events, like starvation, enhanced metabolic demand, cold or heat, not only potentiates inflammation but may also directly trigger it in the absence of PAMPs or DAMPs. Stress-mediated inflammation is also a common feature of many hereditary disorders, due to the proteotoxic effects of mutant proteins. We propose that harmful mutant proteins can induce dysregulated IL-1β production and inflammation through different pathways depending on the cell type involved. When expressed in professional inflammatory cells, stress induced by the mutant protein activates in a cell-autonomous way the onset of inflammation and mediates its aberrant development, resulting in the explosive responses that hallmark autoinflammatory diseases. When expressed in non-immune cells, the mutant protein may cause the release of transcellular stress signals that trigger and propagate inflammation.

Indexed as

autoinflammatory syndromesendoplasmic reticulum stressIL-1βinflammationmonocytesNLRP3 inflammasomeoxidative stresstoll-like receptor

Identifiers

PMID28421072
PMCPMC5378711
OpenAlexW2604264332

What OpenQuestion holds

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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.