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ID 115056
Author
Lee, Youngae Research Institute for Microbial Diseases|WPI Immunology Frontier Research Center
Sasai, Miwa Research Institute for Microbial Diseases|WPI Immunology Frontier Research Center
Ma, Ji Su Research Institute for Microbial Diseases|WPI Immunology Frontier Research Center
Sakaguchi, Naoya Research Institute for Microbial Diseases|WPI Immunology Frontier Research Center
Ohshima, Jun Research Institute for Microbial Diseases|WPI Immunology Frontier Research Center
Bando, Hironori Research Institute for Microbial Diseases|WPI Immunology Frontier Research Center
Saitoh, Tatsuya Research Institute for Microbial Diseases|WPI Immunology Frontier Research Center|Tokushima University KAKEN Search Researchers
Akira, Shizuo Research Institute for Microbial Diseases|WPI Immunology Frontier Research Center
Yamamoto, Masahiro Research Institute for Microbial Diseases|WPI Immunology Frontier Research Center
Content Type
Journal Article
Description
Also known as Sqstm1, p62 is a selective autophagy adaptor with a ubiquitin-binding domain. However, the role of p62 in the host defense against Toxoplasma gondii infection is unclear. Here, we show that interferon γ (IFN-γ) stimulates ubiquitin and p62 recruitment to T. gondii parasitophorous vacuoles (PVs). Some essential autophagy-related proteins, but not all, are required for this recruitment. Regardless of normal IFN-γ-induced T. gondii clearance activity and ubiquitination, p62 deficiency in antigen-presenting cells (APCs) and mice diminishes the robust IFN-γ-primed activation of CD8+ T cells that recognize the T. gondii-derived antigen secreted into PVs. Because the expression of Atg3 and Irgm1/m3 in APCs is essential for PV disruption, ubiquitin and p62 recruitment, and vacuolar-antigen-specific CD8+ T cell activation, IFN-γ-mediated ubiquitination and the subsequent recruitment of p62 to T. gondii are specifically required for the acquired immune response after PV disruption by IFN-γ-inducible GTPases.
Journal Title
Cell Reports
ISSN
22111247
Publisher
Elsevier
Volume
13
Issue
2
Start Page
223
End Page
233
Published Date
2015-10-01
Rights
This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
EDB ID
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Publisher
departments
Institute of Advanced Medical Sciences