Adenosine receptor A2a blockade by caffeine increases IFN-gamma production in Th1 cells from patients with rheumatoid arthritis.


Journal

Scandinavian journal of rheumatology
ISSN: 1502-7732
Titre abrégé: Scand J Rheumatol
Pays: England
ID NLM: 0321213

Informations de publication

Date de publication:
07 2022
Historique:
pubmed: 14 1 2022
medline: 29 6 2022
entrez: 13 1 2022
Statut: ppublish

Résumé

Studies indicate that caffeine uptake may be a risk factor for rheumatoid arthritis (RA), but a definitive link between caffeine consumption and RA has not been established. This study aimed to investigate the interplay between caffeine, adenosine receptor A2a, and interferon-γ (IFN-γ) production in CD4 Peripheral blood mononuclear cells were obtained from the peripheral blood of healthy individuals and patients with RA. CD4 Caffeine promoted IFN-γ production in Th1 cells in vitro. Significantly higher concentrations of caffeine were required to increase IFN-γ levels in Th1 cells from healthy individuals compared to Th1 cells from patients with RA. Moreover, ex vivo levels of adenosine receptor A2a expression on CD4 Caffeine promotes IFN-γ production in Th1 cells from RA patients in vitro by competitive inhibition of adenosine receptor A2a. Excessive coffee consumption could contribute to T-cell activation and inflammation in RA.

Identifiants

pubmed: 35023427
doi: 10.1080/03009742.2021.1995956
doi:

Substances chimiques

Adenosine A2 Receptor Antagonists 0
Caffeine 3G6A5W338E
Interferon-gamma 82115-62-6

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

279-283

Auteurs

L Gloyer (L)

Laboratory of Molecular Immunology, Department I of Internal Medicine, University of Cologne, Cologne, Germany.

V Golumba-Nagy (V)

Laboratory of Molecular Immunology, Department I of Internal Medicine, University of Cologne, Cologne, Germany.

A Meyer (A)

Laboratory of Molecular Immunology, Department I of Internal Medicine, University of Cologne, Cologne, Germany.

S Yan (S)

Laboratory of Molecular Immunology, Department I of Internal Medicine, University of Cologne, Cologne, Germany.

J Schiller (J)

Division of Clinical Immunology and Rheumatology, Department I of Internal Medicine, University of Cologne, and Center for Integrated Oncology Aachen Bonn Cologne Duesseldorf, Cologne, Germany.

M Breuninger (M)

Division of Clinical Immunology and Rheumatology, Department I of Internal Medicine, University of Cologne, and Center for Integrated Oncology Aachen Bonn Cologne Duesseldorf, Cologne, Germany.

D Jochimsen (D)

Division of Clinical Immunology and Rheumatology, Department I of Internal Medicine, University of Cologne, and Center for Integrated Oncology Aachen Bonn Cologne Duesseldorf, Cologne, Germany.

D M Kofler (DM)

Laboratory of Molecular Immunology, Department I of Internal Medicine, University of Cologne, Cologne, Germany.
Division of Clinical Immunology and Rheumatology, Department I of Internal Medicine, University of Cologne, and Center for Integrated Oncology Aachen Bonn Cologne Duesseldorf, Cologne, Germany.

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Classifications MeSH