Autophagy inhibition and mitochondrial remodeling join forces to amplify apoptosis in activation-induced cell death. Issue 12 (1st December 2016)

• Record Type: Journal Article
• Authors: Corrado, Mauro; Campello, Silvia
• Is Part Of: Autophagy. Volume 12:Issue 12(2016)
• Page Start: 2496
• Page End: 2497
• Publication Date: 2016-12-01
• Subjects: AICD -- apoptosis -- autophagy -- mitochondria -- mitochondrial dynamics -- T cells; Autophagic vacuoles -- Periodicals; Apoptosis -- Periodicals; Cell death -- Periodicals; Lysosomes -- Periodicals; Degeneration (Pathology) -- Periodicals; Autophagy -- Periodicals; Cell Death -- Periodicals; Lysosomes -- Periodicals; Periodicals; 571.936
• DOI: 10.1080/15548627.2016.1226738
• Languages: English
• ISSNs: 1554-8627

Abstract

ABSTRACT: Mitochondrial structural and functional changes and the autophagy pathway crosstalk under several stress conditions. However, their interplay under physiological cell death stimulation has been unclear. In our recent report, we show that during activation-induced cell death (AICD), the T-cell receptor (TCR)-dependent pathway that controls immune tolerance, autophagy is inhibited at an early stage. Further, we found that this inhibition is coupled with mitochondria fragmentation and cristae remodeling to unleash the apoptotic program. Last, we dissected the role of macroautophagy/autophagy versus mitophagy in the context of this physiological cell death, and bulk autophagy turned out to be able to remove dysfunctional and depolarized mitochondria. Our data suggest new possible approaches to modulate the immune function in the context of autoimmunity or immunotherapy.