Evidence map›Paper›PMID 33861848›Full record

ArticleThe Journal of experimental medicine2021

Macroautophagy in lymphatic endothelial cells inhibits T cell-mediated autoimmunity.

Guillaume Harlé, Camille Kowalski, Juan Dubrot, Dale Brighouse, Gaëlle Clavel, Robert Pick, Natacha Bessis, Jennifer Niven, Christoph Scheiermann, Monique Gannagé and 1 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Endothelial cell-specific knockout of ATG5 ameliorates inflammation and renal fibrosis by regulating pyroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  13. CD4Nature cancer · 2023
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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

11 authors at 3 institutions in 2 countries.

Guillaume HarléDepartment of Pathology and Immunology, School of Medicine, University of Geneva, Geneva, Switzerland.
Camille KowalskiDepartment of Pathology and Immunology, School of Medicine, University of Geneva, Geneva, Switzerland.
Juan DubrotDepartment of Pathology and Immunology, School of Medicine, University of Geneva, Geneva, Switzerland.
Dale BrighouseDepartment of Pathology and Immunology, School of Medicine, University of Geneva, Geneva, Switzerland.
Gaëlle ClavelInstitut National de la Santé et de la Recherche Médicale, UMR 1125, Université Sorbonne Paris Cité, Université Paris, Paris, France.
Robert PickDepartment of Pathology and Immunology, School of Medicine, University of Geneva, Geneva, Switzerland.
Natacha BessisService of Immunology and Allergy, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Jennifer NivenDepartment of Pathology and Immunology, School of Medicine, University of Geneva, Geneva, Switzerland.
Christoph ScheiermannDepartment of Pathology and Immunology, School of Medicine, University of Geneva, Geneva, Switzerland.
Monique Gannagé *Service of Immunology and Allergy, Lausanne University Hospital, University of Lausanne, Lausanne, Switzerland.
Stéphanie Hugues *Department of Pathology and Immunology, School of Medicine, University of Geneva, Geneva, Switzerland.
University of Geneva · CHUniversity of Lausanne · CHInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lymphatic endothelial cells (LECs) present peripheral tissue antigens to induce T cell tolerance. In addition, LECs are the main source of sphingosine-1-phosphate (S1P), promoting naive T cell survival and effector T cell exit from lymph nodes (LNs). Autophagy is a physiological process essential for cellular homeostasis. We investigated whether autophagy in LECs modulates T cell activation in experimental arthritis. Whereas genetic abrogation of autophagy in LECs does not alter immune homeostasis, it induces alterations of the regulatory T cell (T reg cell) population in LNs from arthritic mice, which might be linked to MHCII-mediated antigen presentation by LECs. Furthermore, inflammation-induced autophagy in LECs promotes the degradation of Sphingosine kinase 1 (SphK1), resulting in decreased S1P production. Consequently, in arthritic mice lacking autophagy in LECs, pathogenic Th17 cell migration toward LEC-derived S1P gradients and egress from LNs are enhanced, as well as infiltration of inflamed joints, resulting in exacerbated arthritis. Our results highlight the autophagy pathway as an important regulator of LEC immunomodulatory functions in inflammatory conditions.

Indexed as

AnimalsArthritisAutoimmunityCell MovementCells, CulturedEndothelial CellsHumansImmune ToleranceInflammationLymphatic VesselsLymph NodesLysophospholipidsMacroautophagyMiceMice, Inbred C57BLSphingosineLysophospholipidsSphingosinesphingosine 1-phosphate

Identifiers

PMID33861848
PMCPMC8056750
OpenAlexW3152889892

What OpenQuestion holds

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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.