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Dimitrov, S. ; Lange, T.* ; Gouttefangeas, C.* ; Jensen, A.T.R.* ; Szczepanski, M.* ; Lehnnolz, J.* ; Soekadar, S.* ; Rammensee, H.G.* ; Born, J. ; Besedovsky, L.*

Gαs-coupled receptor signaling and sleep regulate integrin activation of human antigen-specific T cells.

J. Exp. Med. 216, 517-526 (2019)
Verlagsversion DOI PMC
Open Access Gold (Paid Option)
Creative Commons Lizenzvertrag
Efficient T cell responses require the firm adhesion of T cells to their targets, e.g., virus-infected cells, which depends on T cell receptor (TCR)-mediated activation of beta(2)-integrins. G alpha(s)-coupled receptor agonists are known to have immunosuppressive effects, but their impact on TCR-mediated integrin activation is unknown. Using multimers of peptide major histocompatibility complex molecules (pMHC) and of ICAM-1-the ligand of beta(2)-integrins-we show that the G alpha(s)-coupled receptor agonists isoproterenol, epinephrine, norepinephrine, prostaglandin (PG) E-2, PGD(2), and adenosine strongly inhibit integrin activation on human CMV- and EBV-specific CD8(+) T cells in a dose-dependent manner. In contrast, sleep, a natural condition of low levels of G alpha(s)-coupled receptor agonists, up-regulates integrin activation compared with nocturnal wakefulness, a mechanism possibly underlying some of the immune-supportive effects of sleep. The findings are also relevant for several pathologies associated with increased levels of G alpha(s)-coupled receptor agonists (e.g., tumor growth, malaria, hypoxia, stress, and sleep disturbances).
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Korrespondenzautor
Schlagwörter Cd4+and Cd8+t Cells; Cytokine Production; Immune-responses; In-vitro; Inhibition; Adenosine; Adhesion; Proliferation; Cytotoxicity; Inflammation
ISSN (print) / ISBN 0022-1007
e-ISSN 1540-9538
Zeitschrift Journal of Experimental Medicine
Quellenangaben Band: 216, Heft: 3, Seiten: 517-526 Artikelnummer: , Supplement: ,
Verlag Rockefeller University Press
Verlagsort 950 Third Ave, 2nd Flr, New York, Ny 10022 Usa
Nichtpatentliteratur Publikationen
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Diabetes Research and Metabolic Diseases (IDM)