MDPI Acta Medica Okayama 2073-4409 9 8 2020 Ligation of MHC Class II Induces PKC-Dependent Clathrin-Mediated Endocytosis of MHC Class II 1810 EN Kento Masaki Department of Immunobiology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences Yuhji Hiraki Department of Immunobiology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences Hiroka Onishi Department of Immunobiology, Faculty of Pharmacy and Pharmaceutical Sciences, Okayama University Yuka Satoh Department of Immunobiology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences Paul A. Roche Experimental Immunology Branch, National Cancer Institute, National Institutes of Health Satoshi Tanaka Department of Pharmacology, Division of Pathological Sciences, Kyoto Pharmaceutical University Kazuyuki Furuta Department of Immunobiology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences 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. No potential conflict of interest relevant to this article was reported.

岡山医学会 Acta Medica Okayama 0030-1558 100 11-12 1988 胸腔内原発のhemangiopericytomaの1例 ―(67)Gaシンチグラフィーと病理所見の対比― 1029 1034 EN Masatada Tanabe Fuminori Gohda Midori Yoden Kazuhiro Sakamoto Tsutomu Miyamoto Hiroyuki Seo Yukiko Kawasaki Satoshi Ohkawa Toyosato Tamai Shinya Yamamoto Satoshi Tanaka Shouji Kobayashi A 27-year-old male was admitted to our hospital with the chief complaint of dyspnea. Radiologically, he was found to have a large tumor shadow in the left hemithorax with pleural effusion. The first thoracotomy was done to resect the tumor on January 14, 1988. The second and third thoracotomies were done because of local recurrence in the left hemithorax. Histological diagnosis was of a hmangio-pericytoma. Before the third operation, Ga-67 scintigraphy was performed. Ga-67 accumulation was noted in parts of the tumor mass. Histological findings of the resected tumor were compared with the degree and location of Ga-67 accumulation. Histologically, Ga-67 accumulation occurred in areas of bleeding and necrosis in the tumor tissue, but not in viable parts of the tumor. Ga-67 accumulation usually occurs in viable tumor cells, but our findings were contrary to this generality. No potential conflict of interest relevant to this article was reported.