Evidence map›Paper›PMID 35514976›Full record

ArticleFrontiers in immunology2022

PI3K Signaling in Dendritic Cells Aggravates DSS-Induced Colitis.

Mario Kuttke, Dominika Hromadová, Ceren Yildirim, Julia S Brunner, Andrea Vogel, Hannah Paar, Sophie Peters, Maria Weber, Melanie Hofmann, Martina Kerndl and 9 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

7 citing papers in PubMed, 8 citations in OpenAlex.

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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

19 authors at 3 institutions in 1 country.

Mario KuttkeInstitute for Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Dominika HromadováInstitute for Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Ceren YildirimInstitute for Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Julia S BrunnerInstitute for Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Andrea VogelInstitute for Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Hannah PaarInstitute for Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Sophie PetersInstitute for Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Maria WeberInstitute for Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Melanie HofmannInstitute for Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Martina KerndlInstitute for Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Markus KielerInstitute for Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Hannes DatlerInstitute for Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Laszlo MusiejovskyInstitute for Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Manuel SalzmannInstitute for Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Michaela LangDepartment of Gastroenterology and Hepatology, Internal Medicine III, Medical University of Vienna, Vienna, Austria.
Klara SoukupSt. Anna Children's Cancer Research Institute, Vienna, Austria.
Angela HalfmannSt. Anna Children's Cancer Research Institute, Vienna, Austria.
Omar SharifInstitute for Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Gernot SchabbauerInstitute for Vascular Biology and Thrombosis Research, Center for Physiology and Pharmacology, Medical University of Vienna, Vienna, Austria.
Medical University of Vienna · ATSt. Anna Children's Cancer Research InstituteSt Anna Children's Hospital · AT

Funding

Austrian Science Fund FWF P 24802Austrian Science Fund FWF P 30026Austrian Science Fund FWF P 31106
6 · The paper itself

Abstract

Aberrant innate immune responses to the gut microbiota are causally involved in the pathogenesis of inflammatory bowel diseases (IBD). The exact triggers and main signaling pathways activating innate immune cells and how they modulate adaptive immunity in IBD is still not completely understood. Here, we report that the PI3K/PTEN signaling pathway in dendritic cells enhances IL-6 production in a model of DSS-induced colitis. This results in exacerbated Th1 cell responses and increased mortality in DC-specific PTEN knockout (PTEN

Indexed as

ColitisInflammatory Bowel DiseasesAnimalsDendritic CellsDextran SulfateDisease Models, AnimalInterleukin-6MiceMice, Inbred C57BLPhosphatidylinositol 3-KinasesSignal TransductionDextran SulfateInterleukin-6Phosphatidylinositol 3-Kinasesdendritic cellsDSS-induced colitisInterleukin-6PI3KPTENTh1-response

Identifiers

PMID35514976
PMCPMC9063450
OpenAlexW4224295891

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.