Carregant...
Tipus de document
ArticleVersió
Versió publicadaData de publicació
Llicència de publicació
Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/206103
Antitumor T‐cell function requires CPEB4‐mediated adaptation to chronic endoplasmic reticulum stress
Títol de la revista
Director/Tutor
ISSN de la revista
Títol del volum
Recurs relacionat
Resum
Tumor growth is influenced by a complex network of interactions between multiple cell types in the tumor microenvironment (TME). These constrained conditions trigger the endoplasmic reticulum (ER) stress response, which extensively reprograms mRNA translation. When uncontrolled over time, chronic ER stress impairs the antitumor effector function of CD8 T lymphocytes. How cells promote adaptation to chronic stress in the TME without the detrimental effects of the terminal unfolded protein response (UPR) is unknown. Here, we find that, in effector CD8 T lymphocytes, RNA-binding protein CPEB4 constitutes a new branch of the UPR that allows cells to adapt to sustained ER stress, yet remains decoupled from the terminal UPR. ER stress, induced during CD8 T-cell activation and effector function, triggers CPEB4 expression. CPEB4 then mediates chronic stress adaptation to maintain cellular fitness, allowing effector molecule production and cytotoxic activity. Accordingly, this branch of the UPR is required for the antitumor effector function of T lymphocytes, and its disruption in these cells exacerbates tumor growth.© 2023 The Authors. Published under the terms of the CC BY NC ND 4.0 license.
Matèries (anglès)
Citació
Citació
FERNÁNDEZ ALFARA, Marcos, SIBILIO, Annarita, MARTÍN, Judit, TUSQUETS UXÓ, Elsa, MALUMBRES, Marcos, ALCALDE, Victor, CHANES, Verónica, CAÑELLAS SOCIAS, Adrià, PALOMO PONCE, Sergio, BATLLE, Eduard, MÉNDEZ, Raul. Antitumor T‐cell function requires CPEB4‐mediated adaptation to chronic endoplasmic reticulum stress. _Embo Journal_. 2023. Vol. 42, núm. 9. [consulta: 23 de gener de 2026]. ISSN: 1460-2075. [Disponible a: https://hdl.handle.net/2445/206103]