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Novel regulation of MHC class II function in B cells
Author(s) -
Matsuki Yohei,
OhmuraHoshino Mari,
Goto Eiji,
Aoki Masami,
MitoYoshida Mari,
Uematsu Mika,
Hasegawa Takanori,
Koseki Haruhiko,
Ohara Osamu,
Nakayama Manabu,
Toyooka Kiminori,
Matsuoka Ken,
Hotta Hak,
Yamamoto Akitsugu,
Ishido Satoshi
Publication year - 2007
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/sj.emboj.7601556
Subject(s) - ubiquitin , ubiquitin ligase , mhc class ii , mhc class i , major histocompatibility complex , microbiology and biotechnology , mhc restriction , antigen , biology , cd1 , antigen processing , antigen presenting cell , chemistry , immune system , immunology , t cell , genetics , gene
The presence of post‐translational regulation of MHC class II (MHC II) under physiological conditions has been demonstrated recently in dendritic cells (DCs) that potently function as antigen‐presenting cells (APCs). Here, we report that MARCH‐I, an E3 ubiquitin ligase, plays a pivotal role in the post‐translational regulation of MHC II in B cells. MARCH‐I expression was particularly high in B cells, and the forced expression of MARCH‐I induced the ubiquitination of MHC II. In B cells from MARCH‐I‐deficient mice (MARCH‐I KO), the half‐life of surface MHC II was prolonged and the ubiquitinated form of MHC II completely disappeared. In addition, MARCH‐I‐deficient B cells highly expressed exogenous antigen‐loaded MHC II on their surface and showed high ability to present exogenous antigens. These results suggest that the function of MHC II in B cells is regulated through ubiquitination by MARCH‐I.