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Dudek, M.* ; Lohr, K.* ; Donakonda, S.* ; Baumann, T.* ; Lüdemann, M.* ; Hegenbarth, S.* ; Dübbel, L.* ; Eberhagen, C. ; Michailidou, S.* ; Yassin, A.* ; Prinz, M.* ; Popper, B.* ; Rose-John, S.* ; Zischka, H. ; Knolle, P.A.*

IL-6-induced FOXO1 activity determines the dynamics of metabolism in CD8 T cells cross-primed by liver sinusoidal endothelial cells.

Cell Rep. 38:110389 (2022)
Verlagsversion Forschungsdaten DOI PMC
Open Access Gold
Creative Commons Lizenzvertrag
Liver sinusoidal endothelial cells (LSECs) are liver-resident antigen (cross)-presenting cells that generate memory CD8 T cells, but metabolic properties of LSECs and LSEC-primed CD8 T cells remain understudied. Here, we report that high-level mitochondrial respiration and constitutive low-level glycolysis support LSEC scavenger and sentinel functions. LSECs fail to increase glycolysis and co-stimulation after TLR4 activation, indicating absence of metabolic and functional maturation compared with immunogenic dendritic cells. LSEC-primed CD8 T cells show a transient burst of oxidative phosphorylation and glycolysis. Mechanistically, co-stimulatory IL-6 signaling ensures high FOXO1 expression in LSEC-primed CD8 T cells, curtails metabolic activity associated with T cell activation, and is indispensable for T cell functionality after re-activation. Thus, distinct immunometabolic features characterize non-immunogenic LSECs compared with immunogenic dendritic cells and LSEC-primed CD8 T cells with memory features compared with effector CD8 T cells. This reveals local features of metabolism and function of T cells in the liver.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Glycolysis ; Immune Cell Metabolism ; Liver Immune Tolerance ; Memory T Cells ; Mitochondrial Respiration ; Non-professional Antigen-presenting Cells; Transcription Factors; Energy-metabolism; Dendritic Cell; Memory; Effector; Antigen; Differentiation; Expression; Maturation; Pathway
Sprache englisch
Veröffentlichungsjahr 2022
HGF-Berichtsjahr 2022
ISSN (print) / ISBN 2211-1247
e-ISSN 2211-1247
Zeitschrift Cell Reports
Quellenangaben Band: 38, Heft: 7, Seiten: , Artikelnummer: 110389 Supplement: ,
Verlag Cell Press
Verlagsort 50 Hampshire St, Floor 5, Cambridge, Ma 02139 Usa
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Molecular Toxicology and Pharmacology (TOX)
POF Topic(s) 30203 - Molecular Targets and Therapies
Forschungsfeld(er) Enabling and Novel Technologies
PSP-Element(e) G-505200-003
Förderungen German Center for Infection Research, Munich branch
DFG
DOI 10.1016/j.celrep.2022.110389
WOS ID WOS:000759401700004
Scopus ID 85124528626
PubMed ID 35172161
Erfassungsdatum 2022-05-05
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