start-ver=1.4
cd-journal=joma
no-vol=9
cd-vols=
no-issue=8
article-no=
start-page=1810
end-page=
dt-received=
dt-revised=
dt-accepted=
dt-pub-year=2020
dt-pub=20200730
dt-online=
en-article=
kn-article=
en-subject=
kn-subject=
en-title=
kn-title=Ligation of MHC Class II Induces PKC-Dependent Clathrin-Mediated Endocytosis of MHC Class II
en-subtitle=
kn-subtitle=
en-abstract=
kn-abstract=In addition to antigen presentation to CD4(+)T cells, aggregation of cell surface major histocompatibility complex class II (MHC-II) molecules induces signal transduction in antigen presenting cells that regulate cellular functions. We previously reported that crosslinking of MHC-II induced the endocytosis of MHC-II, which was associated with decreased surface expression levels in murine dendritic cells (DCs) and resulted in impaired activation of CD4(+)T cells. However, the downstream signal that induces MHC-II endocytosis remains to be elucidated. In this study, we found that the crosslinking of MHC-II induced intracellular Ca(2+)mobilization, which was necessary for crosslinking-induced MHC-II endocytosis. We also found that these events were suppressed by inhibitors of Syk and phospholipase C (PLC). Treatments with a phorbol ester promoted MHC-II endocytosis, whereas inhibitors of protein kinase C (PKC) suppressed crosslinking-induced endocytosis of MHC-II. These results suggest that PKC could be involved in this process. Furthermore, crosslinking-induced MHC-II endocytosis was suppressed by inhibitors of clathrin-dependent endocytosis. Our results indicate that the crosslinking of MHC-II could stimulate Ca(2+)mobilization and induce the clathrin-dependent endocytosis of MHC-II in murine DCs.
en-copyright=
kn-copyright=

en-aut-name=MasakiKento
en-aut-sei=Masaki
en-aut-mei=Kento
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=1
ORCID=

en-aut-name=HirakiYuhji
en-aut-sei=Hiraki
en-aut-mei=Yuhji
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=2
ORCID=

en-aut-name=OnishiHiroka
en-aut-sei=Onishi
en-aut-mei=Hiroka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=3
ORCID=

en-aut-name=SatohYuka
en-aut-sei=Satoh
en-aut-mei=Yuka
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=4
ORCID=

en-aut-name=RochePaul A.
en-aut-sei=Roche
en-aut-mei=Paul A.
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=5
ORCID=

en-aut-name=TanakaSatoshi
en-aut-sei=Tanaka
en-aut-mei=Satoshi
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=6
ORCID=

en-aut-name=FurutaKazuyuki
en-aut-sei=Furuta
en-aut-mei=Kazuyuki
kn-aut-name=
kn-aut-sei=
kn-aut-mei=
aut-affil-num=7
ORCID=

affil-num=1
en-affil=Department of Immunobiology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=2
en-affil=Department of Immunobiology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=3
en-affil=Department of Immunobiology, Faculty of Pharmacy and Pharmaceutical Sciences, Okayama University
kn-affil=

affil-num=4
en-affil=Department of Immunobiology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=

affil-num=5
en-affil=Experimental Immunology Branch, National Cancer Institute, National Institutes of Health
kn-affil=

affil-num=6
en-affil=Department of Pharmacology, Division of Pathological Sciences, Kyoto Pharmaceutical University
kn-affil=

affil-num=7
en-affil=Department of Immunobiology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences
kn-affil=
en-keyword=MHC-II
kn-keyword=MHC-II
en-keyword=dendritic cells
kn-keyword=dendritic cells
en-keyword=endocytosis
kn-keyword=endocytosis
en-keyword=crosslink
kn-keyword=crosslink
en-keyword=PKC
kn-keyword=PKC
END