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ABIN1 is a negative regulator of effector functions in cytotoxic T cells

S. Janusova, D. Paprckova, J. Michalik, V. Uleri, A. Drobek, E. Salyova, L. Chorfi, A. Neuwirth, A. Andreyeva, J. Prochazka, R. Sedlacek, P. Draber, O. Stepanek

. 2024 ; 25 (8) : 3456-3485. [pub] 20240614

Jazyk angličtina Země Anglie, Velká Británie

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc24019529

Grantová podpora
22-18046S Grantová Agentura České Republiky (GAČR)
LX22NPO5103 European Union - Next Generation EU
IG 4420 European Molecular Biology Organization (EMBO)
PRIMUS/20/MED/003 Univerzita Karlova v Praze (UK)
984120 Grantová Agentura, Univerzita Karlova (GA UK)
274323 Grantová Agentura, Univerzita Karlova (GA UK)
802878 EC | ERC | HORIZON EUROPE European Research Council (ERC)
OP RDI CZ.1.05/2.1.00/19.0395 Ministerstvo Školství, Mládeže a Tělovýchovy (MŠMT)
LM2023036 Ministerstvo Školství, Mládeže a Tělovýchovy (MŠMT)
OP RDI BIOCEV CZ.1.05/1.1.00/02.0109 Ministerstvo Školství, Mládeže a Tělovýchovy (MŠMT)
LM2023050 Ministerstvo Školství, Mládeže a Tělovýchovy (MŠMT)
RVO - 68378050-KAV-NPUI Ministerstvo Školství, Mládeže a Tělovýchovy (MŠMT)
RVO 68378050 Ústav molekulární genetiky, AVČR core funding

T cells are pivotal in the adaptive immune defense, necessitating a delicate balance between robust response against infections and self-tolerance. Their activation involves intricate cross-talk among signaling pathways triggered by the T-cell antigen receptors (TCR) and co-stimulatory or inhibitory receptors. The molecular regulation of these complex signaling networks is still incompletely understood. Here, we identify the adaptor protein ABIN1 as a component of the signaling complexes of GITR and OX40 co-stimulation receptors. T cells lacking ABIN1 are hyper-responsive ex vivo, exhibit enhanced responses to cognate infections, and superior ability to induce experimental autoimmune diabetes in mice. ABIN1 negatively regulates p38 kinase activation and late NF-κB target genes. P38 is at least partially responsible for the upregulation of the key effector proteins IFNG and GZMB in ABIN1-deficient T cells after TCR stimulation. Our findings reveal the intricate role of ABIN1 in T-cell regulation.

Citace poskytuje Crossref.org

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