Abstract:
:TRAF2 dependent K63-polyubiquitinations have been recently shown to connect CD137 (4-1BB) stimulation to NF-κB activation. In a search of deubiquitinase enzymes (DUBs) that could regulate such a signaling route, A20 and CYLD were found to coimmunoprecipitate with CD137 and TRAF2 complexes. Indeed, overexpression of A20 or CYLD downregulated CD137-elicited ubiquitination of TRAF2 and TAK1 upon stimulation with agonist monoclonal antibodies. Moreover, overexpression of A20 or CYLD downregulated CD137-induced NF-κB activation in cultured cells and in gene-transferred hepatocytes in vivo, while silencing these deubiquitinases enhanced CD137 costimulation of primary human CD8 T cells. Therefore A20 and CYLD directly downregulate the signaling from a T and NK-cell costimulatory receptor under exploitation for cancer immunotherapy in clinical trials.
journal_name
Oncoimmunologyjournal_title
Oncoimmunologyauthors
Azpilikueta A,Bolaños E,Lang V,Labiano S,Aznar MA,Etxeberria I,Teijeira A,Rodriguez-Ruiz ME,Perez-Gracia JL,Jure-Kunkel M,Zapata JM,Rodriguez MS,Melero Idoi
10.1080/2162402X.2017.1368605subject
Has Abstractpub_date
2017-09-21 00:00:00pages
e1368605issue
1eissn
2162-4011issn
2162-402Xpii
1368605journal_volume
7pub_type
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