Fiche publication
Date publication
novembre 2020
Journal
Cancers
Auteurs
Membres identifiés du Cancéropôle Est :
Pr GHIRINGHELLI François
,
Dr REBE Cédric
Tous les auteurs :
Perrichet A, Ghiringhelli F, Rébé C
Lien Pubmed
Résumé
Inflammasomes and immune checkpoints have been shown to participate in carcinogenesis, cancer growth and response to treatment. Thus, targeting cytokines resulting from inflammasome activation, such as interleukin (IL)-1β, has emerged as a new tool in the therapeutic arsenal. Moreover, the use of checkpoint inhibitors such as anti-PD-1 or anti-PD-L1 has revolutionized the treatment of some cancer patients. However, inflammasome activation and consecutive cytokine release only occurs in some chemotherapeutic treatments and immune checkpoint inhibitors only work for a restricted number of patients, thus limiting the use of therapies targeting these pathways. Expanding knowledge about the inefficiency of these therapies recently brought forward the hypothesis of targeting both pathways. In this review, we provide an overview of the crosstalk between inflammasomes and programmed death-1 (PD-1)/programmed death-ligand 1 (PD-L1) that might explain how these two pathways are mutually dependent, and perhaps why targeting only one of them leads to inefficiency of cancer treatment in some patients.
Mots clés
PD-1, PD-L1, cancer, immune checkpoint, inflammasomes, interleukin
Référence
Cancers (Basel). 2020 Nov 27;12(12):
