Evidence map›Paper›PMID 34341503›Full record

ArticleMucosal immunology2021

mTOR signaling mediates ILC3-driven immunopathology.

Claudia Teufel, Edit Horvath, Annick Peter, Caner Ercan, Salvatore Piscuoglio, Michael N Hall, Daniela Finke, Frank M Lehmann

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Mucosal immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

14 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
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  9. Review
  10. ILC3: a case of conflicted identity.Frontiers in immunology · 2023
    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

8 authors at 1 institution in 1 country.

Claudia TeufelDepartment of Biomedicine and University Children's Hospital of Basel, University of Basel, 4058, Basel, Switzerland.
Edit HorvathDepartment of Biomedicine and University Children's Hospital of Basel, University of Basel, 4058, Basel, Switzerland.
Annick PeterDepartment of Biomedicine and University Children's Hospital of Basel, University of Basel, 4058, Basel, Switzerland.
Caner ErcanDepartment of Biomedicine, University of Basel, 4056, Basel, Switzerland.
Salvatore PiscuoglioDepartment of Biomedicine, University of Basel, 4056, Basel, Switzerland.
Michael N HallBiozentrum, University of Basel, 4056, Basel, Switzerland.
Daniela Finke *Department of Biomedicine and University Children's Hospital of Basel, University of Basel, 4058, Basel, Switzerland. daniela.finke@unibas.ch.ORCID 0000-0003-4453-5958
Frank M Lehmann *Department of Biomedicine and University Children's Hospital of Basel, University of Basel, 4058, Basel, Switzerland. f.lehmann@unibas.ch.
University of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Innate lymphoid cells (ILCs) have a protective immune function at mucosal tissues but can also contribute to immunopathology. Previous work has shown that the serine/threonine kinase mammalian target of rapamycin complex 1 (mTORC1) is involved in generating protective ILC3 cytokine responses during bacterial infection. However, whether mTORC1 also regulates IFN-γ-mediated immunopathology has not been investigated. In addition, the role of mTORC2 in ILC3s is unknown. Using mice specifically defective for either mTORC1 or mTORC2 in ILC3s, we show that both mTOR complexes regulate the maintenance of ILC3s at steady state and pathological immune response during colitis. mTORC1 and to a lesser extend mTORC2 promote the proliferation of ILC3s in the small intestine. Upon activation, intestinal ILC3s produce less IFN-γ in the absence of mTOR signaling. During colitis, loss of both mTOR complexes in colonic ILC3s results in the reduced production of inflammatory mediators, recruitment of neutrophils and immunopathology. Similarly, treatment with rapamycin after colitis induction ameliorates the disease. Collectively, our data show a critical role for both mTOR complexes in controlling ILC3 cell numbers and ILC3-driven inflammation in the intestine.

Indexed as

Disease SusceptibilityImmunity, InnateImmunomodulationSignal TransductionAnimalsBiomarkersBone Marrow TransplantationColitisCytokinesDNA-Binding ProteinsImmunophenotypingInflammation MediatorsIntestine, SmallLymphocyte SubsetsMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2BiomarkersCytokinesDNA-Binding ProteinsInflammation MediatorsMechanistic Target of Rapamycin Complex 1Mechanistic Target of Rapamycin Complex 2Rag2 protein, mouseTOR Serine-Threonine Kinases

Identifiers

PMID34341503
PMCPMC8528695
OpenAlexW3192948807

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.