Evidence map›Paper›PMID 27527650›Full record

ArticleAllergy2017

GPR91 deficiency exacerbates allergic contact dermatitis while reducing arthritic disease in mice.

T Rubić-Schneider, N Carballido-Perrig, C Regairaz, L Raad, S Jost, C Rauld, B Christen, G Wieczorek, R Kreutzer, J Dawson and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Allergy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 39 citations in OpenAlex.

  1. Trial
  2. Retiring M1/M2: a view from the succinate receptor.Apoptosis : an international journal on programmed cell death · 2026
    Article
  3. Article
  4. Emerging roles of the metabolite succinate in bone-related diseases.Journal of Zhejiang University. Science. B · 2025
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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

13 authors at 3 institutions in 2 countries.

T Rubić-SchneiderNovartis Institutes for Biomedical Research (NIBR), Basel, Switzerland.
N Carballido-PerrigNovartis Institutes for Biomedical Research (NIBR), Basel, Switzerland.
C RegairazNovartis Institutes for Biomedical Research (NIBR), Basel, Switzerland.
L RaadNovartis Institutes for Biomedical Research (NIBR), Basel, Switzerland.
S JostFormer NIBR, Vienna, Austria.
C RauldNovartis Institutes for Biomedical Research (NIBR), Basel, Switzerland.
B ChristenNovartis Institutes for Biomedical Research (NIBR), Basel, Switzerland.
G WieczorekNovartis Institutes for Biomedical Research (NIBR), Basel, Switzerland.
R KreutzerNovartis Institutes for Biomedical Research (NIBR), Basel, Switzerland.
J DawsonNovartis Institutes for Biomedical Research (NIBR), Basel, Switzerland.
G LametschwandnerFormer NIBR, Vienna, Austria.
A Littlewood-EvansNovartis Institutes for Biomedical Research (NIBR), Basel, Switzerland.
J M CarballidoNovartis Institutes for Biomedical Research (NIBR), Basel, Switzerland.
Novartis Institutes for BioMedical ResearchNovartis (Switzerland) · CHUniversity of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSuccinate, in addition to its role as an intermediary of the citric acid cycle, acts as an alarmin, initiating and propagating danger signals resulting from tissue injury or inflammatory stimuli. The contribution of this immune sensing pathway to the development of allergic and inflammatory responses is unknown.

methodsEar thickness of wild-type (wt) and Sucnr1-deficient (Sucnr1

resultsWe found augmented ACD reactions in Sucnr1

conclusionsA deficiency in succinate sensing during mast cell development confers these cells with a hyperactive phenotype. Such a phenomenon does not translate into exacerbation of asthma or mast cell-dependent arthritis. On the contrary, the fact that Sucnr1

Indexed as

Gene DeletionGenetic Predisposition to DiseaseAnimalsArthritisBiomarkersCytokinesDermatitis, Allergic ContactDisease Models, AnimalDisease ProgressionGenetic Association StudiesHumansImmunoglobulin EInflammation MediatorsMacrophage ActivationMacrophagesMast CellsBiomarkersCytokinesGPR91 protein, mouseImmunoglobulin EInflammation MediatorsReceptors, G-Protein-Coupledalarminsallergyautoimmunityimmunometabolismsuccinate

Identifiers

PMID27527650
PMCPMC5324651
OpenAlexW2516110055

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.