dc.contributor.author | Jugder, Bat-Erdene | |
dc.contributor.author | Cui, Ye | |
dc.contributor.author | Benamar, Mehdi | |
dc.contributor.author | Schmitz-Abe, Klaus | |
dc.contributor.author | Poondi-Krishnan, Varsha | |
dc.contributor.author | Chen, Qian | |
dc.contributor.author | Fatou, Benoit | |
dc.contributor.author | Fong, Jason | |
dc.contributor.author | Zhong, Yuelin | |
dc.contributor.author | Mehta, Stuti | |
dc.contributor.author | Buyanbat, Altantsetseg | |
dc.contributor.author | EKLİOĞLU, BERAY SELVER | |
dc.contributor.author | Karabiber, Esra | |
dc.contributor.author | BARIŞ, SAFA | |
dc.contributor.author | KIYKIM, AYÇA | |
dc.contributor.author | KELEŞ, SEVGİ | |
dc.contributor.author | Stephen-Victor, Emmanuel | |
dc.contributor.author | Angelini, Claudia | |
dc.contributor.author | Charbonnier, Louis-Marie | |
dc.contributor.author | Chatila, Talal A. | |
dc.date.accessioned | 2023-10-10T10:20:21Z | |
dc.date.available | 2023-10-10T10:20:21Z | |
dc.date.issued | 2022 | |
dc.identifier.citation | Cui Y., Benamar M., Schmitz-Abe K., Poondi-Krishnan V., Chen Q., Jugder B., Fatou B., Fong J., Zhong Y., Mehta S., et al., "A Stk4-Foxp3-NF-kappa B p65 transcriptional complex promotes T-reg cell activation and homeostasis", SCIENCE IMMUNOLOGY, sa.75, 2022 | |
dc.identifier.issn | 2470-9468 | |
dc.identifier.other | av_02509966-e3b9-4ad7-b5a5-6a0774dc5765 | |
dc.identifier.other | vv_1032021 | |
dc.identifier.uri | http://hdl.handle.net/20.500.12627/189185 | |
dc.description.abstract | The molecular programs involved in regulatory T (T-reg) cell activation and homeostasis remain incompletely understood. Here, we show that T cell receptor (TCR) signaling in T-reg cells induces the nuclear translocation of serine/threonine kinase 4 (Stk4), leading to the formation of an Stk4-NF-kappa B p65-Foxp3 complex that regulates Foxp3- and p65-dependent transcriptional programs. This complex was stabilized by Stk4-dependent phosphorylation of Foxp3 on serine-418. Stk4 deficiency in T-reg cells, either alone or in combination with its homolog Stk3, precipitated a fatal autoimmune lymphoproliferative disease in mice characterized by decreased Treg cell p65 expression and nuclear translocation, impaired NF-kappa B p65-Foxp3 complex formation, and defective Treg cell activation. In an adoptive immunotherapy model, overexpression of p65 or the phosphomimetic Foxp3S418E in Stk3/4-deficient T-reg cells ameliorated their immune regulatory defects. Our studies identify Stk4 as an essential TCR-responsive regulator of p65-Foxp3-dependent transcription that promotes T-reg cellmediated immune tolerance. | |
dc.language.iso | eng | |
dc.subject | İmmünoloji | |
dc.subject | Yaşam Bilimleri | |
dc.subject | Temel Bilimler | |
dc.subject | Genel İmmünoloji ve Mikrobiyoloji | |
dc.subject | Yaşam Bilimleri (LIFE) | |
dc.title | A Stk4-Foxp3-NF-kappa B p65 transcriptional complex promotes T-reg cell activation and homeostasis | |
dc.type | Makale | |
dc.relation.journal | SCIENCE IMMUNOLOGY | |
dc.contributor.department | Harvard University , , | |
dc.identifier.issue | 75 | |
dc.contributor.firstauthorID | 4311827 | |