LAT1 enables T cell activation under inflammatory conditions.

Mice Animals Synovial Membrane Arthritis, Rheumatoid T-Lymphocyte Subsets T-Lymphocytes, Regulatory / metabolism Signal Transduction Arthritis, Experimental / genetics CD4-Positive T-Lymphocytes
Amino acids Immunometabolism Inflammation Rheumatoid arthritis T lymphocytes

Journal

Journal of autoimmunity
ISSN: 1095-9157
Titre abrégé: J Autoimmun
Pays: England
ID NLM: 8812164

Informations de publication

Date de publication:
07 2023
Historique:
received: 25 01 2023
revised: 09 03 2023
accepted: 17 03 2023
medline: 15 6 2023
pubmed: 25 5 2023
entrez: 25 5 2023
Statut: ppublish

Résumé

The aim of this study was to assess the L-type amino acid transporter-1 (LAT1) as a possible therapeutic target for rheumatoid arthritis (RA). Synovial LAT1 expression in RA was monitored by immunohistochemistry and transcriptomic datasets. The contribution of LAT1 to gene expression and immune synapse formation was assessed by RNA-sequencing and total internal reflection fluorescent (TIRF) microscopy, respectively. Mouse models of RA were used to assess the impact of therapeutic targeting of LAT1. LAT1 was strongly expressed by CD4

Identifiants

DOI: 10.1016/j.jaut.2023.103031 PMID: 37229811
pubmed: 37229811
pii: S0896-8411(23)00040-9
doi: 10.1016/j.jaut.2023.103031
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

103031

Subventions

Organisme : Versus Arthritis
ID : 21434
Pays : United Kingdom
Organisme : Versus Arthritis
ID : 21430
Pays : United Kingdom
Organisme : Arthritis Research UK
ID : 20298
Pays : United Kingdom
Organisme : Department of Health
ID : BRC-1215-20009
Pays : United Kingdom
Organisme : Wellcome Trust
ID : 100262Z/12/Z
Pays : United Kingdom

Informations de copyright

Copyright © 2023. Published by Elsevier Ltd.

Déclaration de conflit d'intérêts

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Joy Ogbechi (J)

Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, OX3 7FY, Oxford, UK. Electronic address: joy.ogbechi@kennedy.ox.ac.uk.

Helen L Wright (HL)

Department of Musculoskeletal and Ageing Science, Institute of Life Course and Medical Sciences, University of Liverpool, 6 West Derby Street, L7 8TX, Liverpool, UK.

Stefan Balint (S)

Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, OX3 7FY, Oxford, UK.

Louise M Topping (LM)

Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, OX3 7FY, Oxford, UK.

Zec Kristina (Z)

Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, OX3 7FY, Oxford, UK.

Yi-Shu Huang (YS)

Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, OX3 7FY, Oxford, UK.

Eirini Pantazi (E)

Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, OX3 7FY, Oxford, UK.

Maarten Swart (M)

Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, OX3 7FY, Oxford, UK.

Dylan Windell (D)

Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, OX3 7FY, Oxford, UK.

Eros Marin (E)

Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, OX3 7FY, Oxford, UK.

Michael F Wempe (MF)

Department of Pharmaceutical Sciences, University of Colorado Anschutz Medical Campus, Aurora, CO, 80045, USA.

Hitoshi Endou (H)

J-Pharma, Co. Ltd., J-Pharma Co., Ltd. Leading Venture Plaza 1-308, 75-1 Onocho, Tsurumi-ku, Yokohama, 230-0046, Japan.

Andrew M Thomas (AM)

The Royal Orthopaedic Hospital, Birmingham, UK.

Andrew Filer (A)

Rheumatology Research Group and Research Into Inflammatory Arthritis Centre Versus Arthritis, Institute of Inflammation and Ageing, NIHR Birmingham Biomedical Research Centre, University Hospitals Birmingham NHS Foundation Trust, Birmingham, UK.

Trevor W Stone (TW)

Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, OX3 7FY, Oxford, UK.

Alexander J Clarke (AJ)

Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, OX3 7FY, Oxford, UK.

Michael L Dustin (ML)

Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, OX3 7FY, Oxford, UK.

Richard O Williams (RO)

Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, OX3 7FY, Oxford, UK.

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Classifications MeSH

questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › LAT1 enables T cell activation under...
questionsmedicales.fr › Eucaryotes › Animaux › LAT1 enables T cell activation under...
questionsmedicales.fr › Appareil locomoteur › Squelette › Articulations › Capsule articulaire › Membrane synoviale › LAT1 enables T cell activation under...
questionsmedicales.fr › Maladies du système immunitaire › Maladies auto-immunes › Polyarthrite rhumatoïde › LAT1 enables T cell activation under...
questionsmedicales.fr › Systèmes sanguin et immunitaire › Système immunitaire › Leucocytes › Agranulocytes › Lymphocytes › Lymphocytes T › Sous-populations de lymphocytes T › LAT1 enables T cell activation under...
questionsmedicales.fr › Systèmes sanguin et immunitaire › Système immunitaire › Leucocytes › Agranulocytes › Lymphocytes › Lymphocytes T › Sous-populations de lymphocytes T › Lymphocytes T régulateurs › LAT1 enables T cell activation under...
questionsmedicales.fr › Phénomènes physiologiques cellulaires › Transduction du signal › LAT1 enables T cell activation under...
questionsmedicales.fr › Techniques d'investigation › Modèles animaux › Arthrite expérimentale › LAT1 enables T cell activation under...
questionsmedicales.fr › Systèmes sanguin et immunitaire › Système immunitaire › Leucocytes › Agranulocytes › Lymphocytes › Lymphocytes T › Lymphocytes T CD4+ › LAT1 enables T cell activation under...