Regulation of Selective B Cell Autophagy by the Pro-oxidant Adaptor p66SHC.
B lymphocytes
ROS
autophagy
mitophagy
p66SHC
Journal
Frontiers in cell and developmental biology
ISSN: 2296-634X
Titre abrégé: Front Cell Dev Biol
Pays: Switzerland
ID NLM: 101630250
Informations de publication
Date de publication:
2020
2020
Historique:
received:
22
01
2020
accepted:
06
03
2020
entrez:
11
4
2020
pubmed:
11
4
2020
medline:
11
4
2020
Statut:
epublish
Résumé
p66SHC is a pro-oxidant member of the SHC family of protein adaptors that acts as a negative regulator of cell survival. In lymphocytes p66SHC exploits both its adaptor and its reactive oxygen species (ROS)-elevating function to antagonize mitogenic and survival signaling and promote apoptosis. As a result, p66SHC deficiency leads to the abnormal expansion of peripheral T and B cells and lupus-like autoimmunity. Additionally, a defect in p66SHC expression is a hallmark of B cell chronic lymphocytic leukemia, where it contributes to the accumulation of long-lived neoplastic cells. We have recently provided evidence that p66SHC exerts a further layer of control on B cell homeostasis by acting as a new mitochondrial LC3-II receptor to promote the autophagic demise of dysfunctional mitochondria. Here we discuss this finding in the context of the autophagic control of B cell homeostasis, development, and differentiation in health and disease.
Identifiants
pubmed: 32274384
doi: 10.3389/fcell.2020.00193
pmc: PMC7113388
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
193Informations de copyright
Copyright © 2020 Onnis, Cassioli, Finetti and Baldari.
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