Autophagy inhibition and mitochondrial remodeling join forces to amplify apoptosis in activation-induced cell death

Corrado Mauro, Campello Silvia

Research output: Contribution to journalArticle

2 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)1-2
Number of pages2
JournalAutophagy
DOIs
Publication statusAccepted/In press - Sep 30 2016

Fingerprint

Autophagy
Cell Death
Apoptosis
Mitochondria
Mitochondrial Degradation
Immune Tolerance
T-Cell Antigen Receptor
Autoimmunity
Immunotherapy

Keywords

  • AICD
  • apoptosis
  • autophagy
  • mitochondria
  • mitochondrial dynamics
  • T cells

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

Cite this

Autophagy inhibition and mitochondrial remodeling join forces to amplify apoptosis in activation-induced cell death. / Mauro, Corrado; Silvia, Campello.

In: Autophagy, 30.09.2016, p. 1-2.

Research output: Contribution to journalArticle

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