Ryugaku Jinja · Professor Archive
Public Professor Archive
Jun Kasamatsu笠松 純
Kagoshima University · Graduate School of Medical and Dental Sciences · 講師
- Publications
- 4
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- 4
- Keywords
- 8
留学
神社Kagoshima University · Graduate School of Medical and Dental Sciences · 講師
Research keywords免疫学・比較免疫学・免疫遺伝学・Cryptococcus・Microbiology・Yeast・感染における防御免疫応答とその破綻・もやもや病研究の最前線
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- Yamamoto Hideki, Tomiyama Chikako, Sato Ko, Kasamatsu Jun, Takano Kazuki, Umeki Aya, Nakahata Nana, Miyasaka Tomomitsu, Kanno Emi, Tanno Hiromasa, Yamasaki Sho, Saijo Shinobu, Iwakura Yoichiro, Ishii Keiko, Kawakami Kazuyoshi2021 · 記述言語: 英語 出版者・発行元: バイオメディカルリサーチプレス
- Yamamoto Hideki, Tomiyama Chikako, Sato Ko, Kasamatsu Jun, Takano Kazuki, Umeki Aya, Nakahata Nana, Miyasaka Tomomitsu, Kanno Emi, Tanno Hiromasa, Yamasaki Sho, Saijo Shinobu, Iwakura Yoichiro, Ishii記述言語: 英語 出版者・発行元: バイオメディカルリサーチプレス Dectin-2とMincleについて、ヘマグルチニン(HA)を介したインフルエンザウイルス(IFV)の認識と、感染による炎症反応惹起におけるC型レクチン受容体(CLR)の役割を調べた。A型およびB型株由来のHAによる刺激時に、Dectin-2の欠乏により骨髄由来樹状細胞(BM-DC)による炎症性サイトカイン産生が減少したが、Mincleでは減少しなかった。細胞内シグナル伝達分子である脾臓チロシンキナーゼ阻害剤は、HA刺激BM-DCによるサイトカイン合成を抑制した。HAは、コンカナバリンA結合分子により識別されるように、Dectin-2の特定のリガンドを保有していた。以上より、Dectin-2は免疫応答を発動し、IFV感染の病因を調節するためのIFVのセンサーとして重要な分子であると考えられた。
- Comparative genomic analysis of mammalian NKG2D ligand family genes provides insights into their origin and evolution
- Kitai Y., Sato K., Tanno D., Yuan X., Umeki A., Kasamatsu J., Kanno E., Tanno H., Hara H., Yamasaki S., Saijo S., Iwakura Y., Ishii K., Kawakamia K. . Role of Dectin-2 in the phagocytosis of C記述言語: 日本語 出版者・発行元: Infection and Immunity The cell walls and capsules of Cryptococcus neoformans, a yeast-type fungal pathogen, are rich in polysaccharides. Dectin-2 is a C-type lectin receptor (CLR) that recognizes high-mannose polysaccharides. Previously, we demonstrated that Dectin-2 is involved in cytokine production by bone marrow-derived dendritic cells (BM-DCs) in response to stimulation with C. neoformans. In the present study, we analyzed the role of Dectin-2 in the phagocytosis of C. neoformans by BM-DCs. The engulfment of this fungus by BM-DCs was significantly decreased in mice lacking Dectin-2 (Dectin-2 knockout [Dectin-2KO]) or caspase recruitment domain-containing protein 9 (CARD9KO), a common adapter molecule that delivers signals triggered by CLRs, compared to wild-type (WT) mice. Phagocytosis was likewise inhibited, to a similar degree, by the inhibition of Syk, a signaling molecule involved in CLR-triggered activation. A PI3K inhibitor, in contrast, completely abrogated the phagocytosis of C. neoformans. Actin polymerization, i.e., conformational changes in cytoskeletons detected at sites of contact with C. neoformans, was also decreased in BM-DCs of Dectin-2KO and CARD9KO mice. Finally, the engulfment of C. neoformans by macrophages was significantly decreased in the lungs of Dectin-2KO mice compared to WT mice. These results suggest that Dectin-2 may play an important role in the actin polymerization and phagocytosis of C. neoformans by DCs, possibly through signaling via CARD9 and a signaling pathway mediated by Syk and PI3K. DOI: 10.1128/IAI.00330-21 Scopus PubMed
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