2021/12/04 更新

写真a

ヤマモト ヒデキ
山本 秀輝
YAMAMOTO Hideki
所属
教育研究院 医歯学系 保健学系列 助教
医学部 保健学科 助教
職名
助教
外部リンク

学位

  • 保健学 ( 2014年3月   東北大学 )

研究分野

  • ライフサイエンス / 救急医学

  • ライフサイエンス / 免疫学

  • ライフサイエンス / 感染症内科学

経歴(researchmap)

  • 新潟大学   教育研究院医歯学系保健学系列   助教

    2021年4月 - 現在

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    国名:日本国

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  • 新潟大学   研究推進機構 超域学術院   助教

    2020年4月 - 2021年3月

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    国名:日本国

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  • 新潟大学   研究推進機構 超域学術院   特任助教

    2017年1月 - 2020年3月

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経歴

  • 新潟大学   教育研究院 医歯学系 保健学系列   助教

    2021年4月 - 現在

  • 新潟大学   研究推進機構 超域学術院   助教

    2020年4月 - 2021年3月

  • 新潟大学   研究推進機構 超域学術院   特任助教

    2017年1月 - 2020年3月

学歴

  • 東北大学   大学院医学系研究科   保健学専攻 博士後期課程 修了

    - 2014年3月

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    国名: 日本国

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所属学協会

取得資格

  • 臨床検査技師

 

論文

  • Deficiency of lung-specific claudin-18 leads to aggravated infection with Cryptococcus deneoformans through dysregulation of the microenvironment in lungs 査読

    Ko Sato, Ikumi Matsumoto, Koya Suzuki, Atsushi Tamura, Aki Shiraishi, Hiroshi Kiyonari, Jun Kasamatsu, Hideki Yamamoto, Tomomitsu Miyasaka, Daiki Tanno, Anna Miyahara, Tong Zong, Takafumi Kagesawa, Akiho Oniyama, Kotone Kawamura, Yuki Kitai, Aya Umeki, Emi Kanno, Hiromasa Tanno, Keiko Ishii, Sachiko Tsukita, Kazuyoshi Kawakami

    Scientific Reports   11 ( 1 )   21110 - 21110   2021年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Springer Science and Business Media LLC  

    <title>Abstract</title><italic>Cryptococcus deneoformans</italic> is an opportunistic fungal pathogen that infects the lungs via airborne transmission and frequently causes fatal meningoencephalitis. Claudins (Cldns), a family of proteins with 27 members found in mammals, form the tight junctions within epithelial cell sheets. Cldn-4 and 18 are highly expressed in airway tissues, yet the roles of these claudins in respiratory infections have not been clarified. In the present study, we analyzed the roles of Cldn-4 and lung-specific Cldn-18 (luCldn-18) in host defense against <italic>C. deneoformans</italic> infection. luCldn-18-deficient mice exhibited increased susceptibility to pulmonary infection, while Cldn-4-deficient mice had normal fungal clearance. In luCldn-18-deficient mice, production of cytokines including IFN-γ was significantly decreased compared to wild-type mice, although infiltration of inflammatory cells including CD4<sup>+</sup> T cells into the alveolar space was significantly increased. In addition, luCldn-18 deficiency led to high K<sup>+</sup> ion concentrations in bronchoalveolar lavage fluids and also to alveolus acidification. The fungal replication was significantly enhanced both in acidic culture conditions and in the alveolar spaces of luCldn-18-deficient mice, compared with physiological pH conditions and those of wild-type mice, respectively. These results suggest that luCldn-18 may affect the clinical course of cryptococcal infection indirectly through dysregulation of the alveolar space microenvironment.

    DOI: 10.1038/s41598-021-00708-6

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    その他リンク: https://www.nature.com/articles/s41598-021-00708-6

  • Dectin-2-mediated initiation of immune responses caused by influenza virus hemagglutinin 査読

    Hideki Yamamoto, Chikako Tomiyama, Ko Sato, Jun Kasamatsu, Kazuki Takano, Aya Umeki, Nana Nakahata, Tomomitsu Miyasaka, Emi Kanno, Hiromasa Tanno, Sho Yamasaki, Shinobu Saijo, Yoichiro Iwakura, Keiko Ishii, Kazuyoshi Kawakami

    Biomedical Research   42 ( 2 )   53 - 66   2021年4月

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    担当区分:筆頭著者, 責任著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Biomedical Research Press  

    DOI: 10.2220/biomedres.42.53

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  • Contribution of Invariant Natural Killer T Cells to the Clearance of Pseudomonas aeruginosa from Skin Wounds 査読

    Hiromasa Tanno, Emi Kanno, Suzuna Sato, Yu Asao, Mizuki Shimono, Shiho Kurosaka, Yukari Oikawa, Shinyo Ishi, Miki Shoji, Ko Sato, Jun Kasamatsu, Tomomitsu Miyasaka, Hideki Yamamoto, Keiko Ishii, Yoshimichi Imai, Masahiro Tachi, Kazuyoshi Kawakami

    International Journal of Molecular Sciences   22 ( 8 )   3931 - 3931   2021年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:MDPI AG  

    Chronic infections are considered one of the most severe problems in skin wounds, and bacteria are present in over 90% of chronic wounds. Pseudomonas aeruginosa is frequently isolated from chronic wounds and is thought to be a cause of delayed wound healing. Invariant natural killer T (iNKT) cells, unique lymphocytes with a potent regulatory ability in various inflammatory responses, accelerate the wound healing process. In the present study, we investigated the contribution of iNKT cells in the host defense against P. aeruginosa inoculation at the wound sites. We analyzed the re-epithelialization, bacterial load, accumulation of leukocytes, and production of cytokines and antimicrobial peptides. In iNKT cell–deficient (Jα18KO) mice, re-epithelialization was significantly decreased, and the number of live colonies was significantly increased, when compared with those in wild-type (WT) mice on day 7. IL-17A, and IL-22 production was significantly lower in Jα18KO mice than in WT mice on day 5. Furthermore, the administration of α-galactosylceramide (α-GalCer), a specific activator of iNKT cells, led to enhanced host protection, as shown by reduced bacterial load, and to increased production of IL-22, IL-23, and S100A9 compared that of with WT mice. These results suggest that iNKT cells promote P. aeruginosa clearance during skin wound healing.

    DOI: 10.3390/ijms22083931

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  • Effect of CARD9 deficiency on neutrophil-mediated host defense against pulmonary infection with Streptococcus pneumoniae 査読

    Shigenari Ishizuka, Rin Yokoyama, Ko Sato, Ryuhei Shiroma, Ayako Nakahira, Hideki Yamamoto, Kazuki Takano, Takafumi Kagesawa, Tomomitsu Miyasaka, Jun Kasamatsu, Emi Kanno, Hiromasa Tanno, Keiko Ishii, Kazuyoshi Kawakami

    Infection and Immunity   89 ( 1 )   e00305 - e00320   2020年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:American Society for Microbiology  

    <italic>Streptococcus pneumoniae</italic> is a major causative bacterium of community-acquired pneumonia. Dectin-2, one of the C-type lectin receptors (CLRs), was previously reported to play a pivotal role in host defense against pneumococcal infection through regulating phagocytosis by neutrophils while not being involved in neutrophil accumulation. In the present study, to elucidate the possible contribution of other CLRs to neutrophil accumulation, we examined the role of CARD9, a common adaptor molecule for signal transduction triggered by CLRs, in neutrophilic inflammatory response against pneumococcal infection. Wild-type (WT), CARD9 knockout (KO), and Dectin-2KO mice were infected intratracheally with pneumococcus, and the infected lungs were histopathologically analyzed to assess neutrophil accumulation at 24 h post-infection. Bronchoalveolar lavage fluids (BALFs) were collected at the same time point to count the neutrophils and assess the production of inflammatory cytokines and chemokines. Neutrophil accumulation was significantly decreased in CARD9KO mice, but not in Dectin-2KO mice. TNF-α, KC and MIP-2 production in BALFs were also attenuated in CARD9KO mice, but not in Dectin-2KO mice. Production of TNF-α and KC by alveolar macrophages stimulated with pneumococcal culture supernatants were significantly attenuated in CARD9KO mice, but not in Dectin-2KO mice, compared to each group's respective control mice. In addition, pneumococcus-infected CARD9KO mice showed larger bacterial burdens in the lungs than WT mice. These data indicate that CARD9 is required for neutrophil migration after pneumococcal infection as well as inflammatory cytokine and chemokine production by alveolar macrophages and suggest that a CLR distinct from Dectin-2 may be involved in this response.

    DOI: 10.1128/iai.00305-20

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  • Limited role of Mincle in the host defense against infection with <i>Cryptococcus deneoformans</i> 査読 国際誌

    Yuki Sato, Ko Sato, Hideki Yamamoto, Jun Kasamatsu, Tomomitsu Miyasaka, Daiki Tanno, Anna Miyahara, Takafumi Kagesawa, Akiho Oniyama, Kotone Kawamura, Rin Yokoyama, Yuki Kitai, Shigenari Ishizuka, Kazuki Takano, Ryuhei Shiroma, Nana Nakahata, Kaori Kawakami, Emi Kanno, Hiromasa Tanno, Sho Yamasaki, Hiromitsu Hara, Keiko Ishii, Kazuyoshi Kawakami

    Infection and Immunity   88 ( 11 )   e00400 - e00420   2020年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:American Society for Microbiology  

    <italic>Cryptococcus deneoformans</italic> is an opportunistic fungal pathogen that frequently causes fatal meningoencephalitis in patients with impaired cell-mediated immune responses such as AIDS. Caspase-associated recruitment domain 9 (CARD9) plays a critical role in the host defense against cryptococcal infection, suggesting the involvement of one or more C-type lectin receptors (CLRs). In the present study, we analyzed the role of macrophage-inducible C-type lectin (Mincle), one of the CLRs, in the host defense against <italic>C. deneoformans</italic> infection. Mincle expression in the lungs of wild-type (WT) mice was increased in the early stage of cryptococcal infection in a CARD9-dependent manner. In Mincle gene-disrupted (Mincle KO) mice, the clearance of this fungus, pathological findings, Th1/Th2 response, and antimicrobial peptide production in the infected lungs were nearly comparable to those in WT mice. However, the production of IL-22, TNF-α, and IL-6 and the expression of AhR were significantly decreased in the lungs of Mincle KO mice compared to in WT mice. In <italic>in vitro</italic> experiments, TNF-α production by bone marrow-derived dendritic cells was significantly decreased in Mincle KO mice. In addition, the disrupted lysates of <italic>C. deneoformans</italic>, but not of whole yeast cells, activated Mincle-triggered signaling in an assay with a nuclear factor of activated T cells (NFAT)-green fluorescent protein (GFP) reporter cells expressing this receptor. These results suggest that Mincle may be involved in the production of Th22-related cytokines at the early stage of cryptococcal infection, although its role may be limited in the host defense against infection with <italic>C. deneoformans</italic>.

    DOI: 10.1128/iai.00400-20

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  • Production of IL-17A at Innate Immune Phase Leads to Decreased Th1 Immune Response and Attenuated Host Defense against Infection with <i>Cryptococcus deneoformans</i>. 査読 国際誌

    Ko Sato, Hideki Yamamoto, Toshiki Nomura, Jun Kasamatsu, Tomomitsu Miyasaka, Daiki Tanno, Ikumi Matsumoto, Takafumi Kagesawa, Anna Miyahara, Tong Zong, Akiho Oniyama, Kotone Kawamura, Rin Yokoyama, Yuki Kitai, Shigenari Ishizuka, Emi Kanno, Hiromasa Tanno, Hiromi Suda, Masanobu Morita, Masayuki Yamamoto, Yoichiro Iwakura, Keiko Ishii, Kazuyoshi Kawakami

    Journal of immunology   205 ( 3 )   686 - 698   2020年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    IL-17A is a proinflammatory cytokine produced by many types of innate immune cells and Th17 cells and is involved in the elimination of extracellularly growing microorganisms, yet the role of this cytokine in the host defense against intracellularly growing microorganisms is not well known. Cryptococcus deneoformans is an opportunistic intracellular growth fungal pathogen that frequently causes fatal meningoencephalitis in patients with impaired immune responses. In the current study, we analyzed the role of IL-17A in the host defense against C. deneoformans infection. IL-17A was quickly produced by γδT cells at an innate immune phase in infected lungs. In IL-17A gene-disrupted mice, clearance of this fungal pathogen and the host immune response mediated by Th1 cells were significantly accelerated in infected lungs compared with wild-type mice. Similarly, killing of this fungus and production of inducible NO synthase and TNF-α were significantly enhanced in IL-17A gene-disrupted mice. In addition, elimination of this fungal pathogen, Th1 response, and expression of IL-12Rβ2 and IFN-γ in NK and NKT cells were significantly suppressed by treatment with rIL-17A. The production of IL-12p40 and TNF-α from bone marrow-derived dendritic cells stimulated with C. deneoformans was significantly suppressed by rIL-17A. In addition, rIL-17A attenuated Th1 cell differentiation in splenocytes from transgenic mice highly expressing TCR for mannoprotein 98, a cryptococcal Ag, upon stimulation with recombinant mannoprotein 98. These data suggest that IL-17A may be involved in the negative regulation of the local host defense against C. deneoformans infection through suppression of the Th1 response.

    DOI: 10.4049/jimmunol.1901238

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  • Novel Toll-Like Receptor 9 Agonist Derived from <i>Cryptococcus neoformans</i> Attenuates Allergic Inflammation Leading to Asthma Onset in Mice 査読

    Kaori Dobashi-Okuyama, Kazuyoshi Kawakami, Tomomitsu Miyasaka, Ko Sato, Keiko Ishii, Kaori Kawakami, Chiaki Masuda, Syugo Suzuki, Jun Kasamatsu, Hideki Yamamoto, Daiki Tanno, Emi Kanno, Hiromasa Tanno, Tasuku Kawano, Motoaki Takayanagi, Tomoko Takahashi, Isao Ohno

    International Archives of Allergy and Immunology   181 ( 9 )   651 - 664   2020年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:S. Karger AG  

    DOI: 10.1159/000508535

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  • Dectin-2-mediated signaling triggered by the cell wall polysaccharides of <i>Cryptococcus neoformans</i>. 査読 国際誌

    Daiki Tanno, Rin Yokoyama, Kotone Kawamura, Yuki Kitai, Xiaoliang Yuan, Keiko Ishii, Magdia De Jesus, Hideki Yamamoto, Ko Sato, Tomomitsu Miyasaka, Hiroki Shimura, Nobuyuki Shibata, Yoshiyuki Adachi, Naohito Ohno, Sho Yamasaki, Kazuyoshi Kawakami

    Microbiology and immunology   63 ( 12 )   500 - 512   2019年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Cryptococcus neoformans is rich in polysaccharides of the cell wall and capsule. Dectin-2 recognizes high-mannose polysaccharides and plays a central role in the immune response to fungal pathogens. Previously, we demonstrated Dectin-2 was involved in the activation of dendritic cells upon stimulation with C. neoformans, suggesting the existence of a ligand recognized by Dectin-2. In the present study, we examined the cell wall structures of C. neoformans contributing to the Dectin-2-mediated activation of immune cells. In a NFAT-GFP reporter assay of the reported cells expressing Dectin-2, the lysates, but not the whole yeast cells, of an acapsular strain of C. neoformans (Cap67) delivered Dectin-2-mediated signaling. This activity was detected in the supernatant of β-glucanase-treated Cap67 and more strongly in the semi-purified polysaccharides of this supernatant using ConA-affinity chromatography (ConA-bound fraction), in which a large amount of saccharides, but not protein, were detected. Treatment of this supernatant with periodic acid and the addition of excessive mannose, but not glucose or galactose, strongly inhibited this activity. The ConA-bound fraction of the β-glucanase-treated Cap67 supernatant was bound to Dectin-2-Fc fusion protein in a dose-dependent manner and strongly induced the production of interleukin-12p40 and tumour necrosis factor-α by dendritic cells; this was abrogated under the Dectin-2-deficient condition. Finally, 98 kDa mannoprotein (MP98) derived from C. neoformans showed activation of the reporter cells expressing Dectin-2. These results suggested that a ligand with mannose moieties may exist in the cell walls and play a critical role in the activation of dendritic cells during infection with C. neoformans.

    DOI: 10.1111/1348-0421.12746

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  • Consideration to health care and gender in Sri Lanka: mainly examined themes related to women's health 査読

    Thalwaththe Gedara Nadeeka, Shayamalie Gunarathne, Masaru Nakamura, Hagiko Aoki, Megumi Taguchi, Kaori Hotta, Mayumi Ishida, Yoshihiro Yamazaki, Sayuri Sakai, Momoe Sakagami, Megumi Sato, Takuichi Sato, Hideki Yamamoto, Mitsuya Iwafuchi

    新潟大学保健学雑誌   16 ( 1 )   1 - 10   2019年5月

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    記述言語:英語   掲載種別:研究論文(大学,研究機関等紀要)  

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  • Contribution of CARD9-mediated signalling to wound healing in skin 査読 国際誌

    Emi Kanno, Kazuyoshi Kawakami, Hiromasa Tanno, Aiko Suzuki, Noriko Sato, Airi Masaki, Ayano Imamura, Naoyuki Takagi, Takayuki Miura, Hideki Yamamoto, Keiko Ishii, Hiromitsu Hara, Yoshimichi Imai, Ryoko Maruyama, Masahiro Tachi

    Experimental Dermatology   26 ( 11 )   1097 - 1104   2017年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Wiley  

    The inflammatory response after skin injury involves the secretion of a variety of cytokines and growth factors that are necessary for tissue repair. Caspase recruitment domain-containing protein 9 (CARD9) is an essential signalling adaptor molecule for NF-κB activation upon triggering through C-type lectin receptors (CLRs), which are expressed in macrophages and dendritic cells. However, the role of CARD9 in inflammatory responses at the wound site has not been elucidated. In this study, we analysed the role of CARD9 in the healing process of skin wounds. Wounds were created on the backs of wild-type (WT) C57BL/6 mice and CARD9 gene-disrupted (knockout [KO]) mice. We analysed per cent wound closure, and the wound tissues were harvested for analysis of leucocyte accumulation and cytokine and chemokine expressions. CARD9KO mice exhibited significant attenuation of wound closure compared with WT mice on days 5, 7 and 10 postwounding, which was associated with decreased macrophage accumulation and reduced TNF-α, IL-1β, CCL3 and CCL4 expressions. These results suggest that CARD9 may be involved in the wound-healing process through the regulation of macrophage-mediated inflammatory responses.

    DOI: 10.1111/exd.13389

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  • Invariant NKT cells promote skin wound healing by preventing a prolonged neutrophilic inflammatory response 査読

    Hiromasa Tanno, Kazuyoshi Kawakami, Emi Kanno, Aiko Suzuki, Naoyuki Takagi, Hideki Yamamoto, Keiko Ishii, Yoshimichi Imai, Ryoko Maruyama, Masahiro Tachi

    Wound Repair and Regeneration   25 ( 5 )   805 - 815   2017年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Wiley  

    DOI: 10.1111/wrr.12588

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  • <i>Cryptococcus neoformans</i> Infection in Mice Lacking Type I Interferon Signaling Leads to Increased Fungal Clearance and IL-4-Dependent Mucin Production in the Lungs 査読

    Ko Sato, Hideki Yamamoto, Toshiki Nomura, Ikumi Matsumoto, Tomomitsu Miyasaka, Tong Zong, Emi Kanno, Kazuko Uno, Keiko Ishii, Kazuyoshi Kawakami

    PLoS One   10 ( 9 )   e0138291   2015年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PUBLIC LIBRARY SCIENCE  

    Type I interferons (IFNs) are secreted by many cell types upon stimulation via pattern recognition receptors and bind to IFN-alpha/beta receptor (IFNAR), which is composed of IFNAR1 and IFNAR2. Although type I IFNs are well known as anti-viral cytokines, limited information is available on their role during fungal infection. In the present study, we addressed this issue by examining the effect of IFNAR1 defects on the host defense response to Cryptococcus neoformans. In IFNAR1KO mice, the number of live colonies was lower and the host immune response mediated not only by Th1 but also by Th2 and Th17-related cytokines was more accelerated in the infected lungs than in WT mice. In addition, mucin production by bronchoepithelial cells and expression of MUC5AC, a major core protein of mucin in the lungs, were significantly higher in IFNAR1KO mice than in WT mice. This increase in mucin and MUC5AC production was significantly inhibited by treatment with neutralizing anti-IL-4 mAb. In contrast, administration of recombinant IFN-alpha A/D significantly suppressed the production of IL-4, but not of IFN-gamma and IL-17A, in the lungs of WT mice after cryptococcal infection. These results indicate that defects of IFNAR1 led to improved clearance of infection with C. neoformans and enhanced synthesis of IFN-gamma and the IL-4-dependent production of mucin. They also suggest that type I IFNs may be involved in the negative regulation of early host defense to this infection.

    DOI: 10.1371/journal.pone.0138291

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  • Dectin-2 deficiency promotes Th2 response and mucin production in the lungs after pulmonary infection with <i>Cryptococcus neoformans</i>. 査読 国際誌

    Yuri Nakamura, Ko Sato, Hideki Yamamoto, Kana Matsumura, Ikumi Matsumoto, Toshiki Nomura, Tomomitsu Miyasaka, Keiko Ishii, Emi Kanno, Masahiro Tachi, Sho Yamasaki, Shinobu Saijo, Yoichiro Iwakura, Kazuyoshi Kawakami

    Infection and immunity   83 ( 2 )   671 - 81   2015年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Dectin-2 is a C-type lectin receptor that recognizes high mannose polysaccharides. Cryptococcus neoformans, a yeast-form fungal pathogen, is rich in polysaccharides in its cell wall and capsule. In the present study, we analyzed the role of Dectin-2 in the host defense against C. neoformans infection. In Dectin-2 gene-disrupted (knockout) (Dectin-2KO) mice, the clearance of this fungus and the inflammatory response, as shown by histological analysis and accumulation of leukocytes in infected lungs, were comparable to those in wild-type (WT) mice. The production of type 2 helper T (Th2) cytokines in lungs was higher in Dectin-2KO mice than in WT mice after infection, whereas there was no difference in the levels of production of Th1, Th17, and proinflammatory cytokines between these mice. Mucin production was significantly increased in Dectin-2KO mice, and this increase was reversed by administration of anti-interleukin 4 (IL-4) monoclonal antibody (MAb). The levels of expression of β1-defensin, cathelicidin, surfactant protein A (Sp-A), and Sp-D in infected lungs were comparable between these mice. In in vitro experiments, IL-12p40 and tumor necrosis factor alpha (TNF-α) production and expression of CD86 and major histocompatibility complex (MHC) class II by bone marrow-derived dendritic cells and alveolar macrophages were completely abrogated in Dectin-2KO mice. Finally, the disrupted lysates of C. neoformans, but not of whole yeast cells, activated Dectin-2-triggered signaling in an assay with nuclear factor of activated T cells (NFAT)-green fluorescent protein (GFP) reporter cells expressing this receptor. These results suggest that Dectin-2 may oppose the Th2 response and IL-4-dependent mucin production in the lungs after infection with C. neoformans, and it may not be required for the production of Th1, Th17, and proinflammatory cytokines or for clearance of this fungal pathogen.

    DOI: 10.1128/IAI.02835-14

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  • Defect of CARD9 leads to impaired accumulation of gamma interferon-producing memory phenotype T cells in lungs and increased susceptibility to pulmonary infection with <i>Cryptococcus neoformans</i>. 査読 国際誌

    Hideki Yamamoto, Yuri Nakamura, Ko Sato, Yurie Takahashi, Toshiki Nomura, Tomomitsu Miyasaka, Keiko Ishii, Hiromitsu Hara, Natsuo Yamamoto, Emi Kanno, Yoichiro Iwakura, Kazuyoshi Kawakami

    Infection and immunity   82 ( 4 )   1606 - 15   2014年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Caspase recruitment domain-containing protein 9 (CARD9) is an adaptor molecule signal that is critical for NF-κB activation and is triggered through C-type lectin receptors (CLRs), which are pattern recognition receptors that recognize carbohydrate structures. Previous studies have reported that Cryptococcus neoformans, a fungal pathogen that causes meningoencephalitis in AIDS patients, is recognized through some CLRs, such as mannose receptors or DC-SIGN. However, the role of CARD9 in the host defense against cryptococcal infection remains to be elucidated. In the present study, we analyzed the role of CARD9 in the host defense against pulmonary infection with C. neoformans. CARD9 gene-disrupted (knockout [KO]) mice were highly susceptible to this infection, as shown by the reduced fungal clearance in the infected lungs of CARD9 KO mice, compared to that in wild-type (WT) mice. Gamma interferon (IFN-γ) production was strongly reduced in CARD9 KO mice during the innate-immunity phase of infection. Reduced IFN-γ synthesis was due to impaired accumulation of NK and memory phenotype T cells, which are major sources of IFN-γ innate-immunity-phase production; a reduction in the accumulation of these cells was correlated with reduced CCL4, CCL5, CXCL9, and CXCL10 synthesis. However, differentiation of Th17 cells, but not of Th1 cells, was impaired at the adaptive-immunity phase in CARD9 KO mice compared to WT mice, although there was no significant difference in the infection susceptibility between interleukin 17A (IL-17A) KO and WT mice. These results suggest that CARD9 KO mice are susceptible to C. neoformans infection probably due to the reduced accumulation of IFN-γ-expressing NK and memory phenotype T cells at the early stage of infection.

    DOI: 10.1128/IAI.01089-13

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  • Involvement of Gr-1dull+ Cells in the Production of TNF-α and IL-17 and Exacerbated Systemic Inflammatory Response Caused by Lipopolysaccharide 査読

    Daiki Tanno, Yukiko Akahori, Masahiko Toyama, Ko Sato, Daisuke Kudo, Yuzuru Abe, Tomomitsu Miyasaka, Hideki Yamamoto, Keiko Ishii, Emi Kanno, Ryoko Maruyama, Shigeki Kushimoto, Yoichiro Iwakura, Kazuyoshi Kawakami

    Inflammation   37 ( 1 )   186 - 195   2014年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Springer Science and Business Media LLC  

    DOI: 10.1007/s10753-013-9729-5

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    その他リンク: http://link.springer.com/article/10.1007/s10753-013-9729-5/fulltext.html

  • Involvement of high mobility group box 1 and the therapeutic effect of recombinant thrombomodulin in a mouse model of severe acute respiratory distress syndrome 査読

    Daisuke Kudo, Masahiko Toyama, Tetsuji Aoyagi, Yukiko Akahori, Hideki Yamamoto, Keiko Ishii, Emi Kanno, Ryoko Maruyama, Mitsuo Kaku, Shigeki Kushimoto, Kazuyoshi Kawakami

    Clinical & Experimental Immunology   173 ( 2 )   276 - 287   2013年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Wiley  

    DOI: 10.1111/cei.12106

    PubMed

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  • Continuous hydrothermal synthesis of 3,4-dihydroxyhydrocinnamic acid-modified magnetite nanoparticles with stealth-functionality against immunological response 査読

    Takanari Togashi, Seiichi Takami, Kazuyoshi Kawakami, Hideki Yamamoto, Takashi Naka, Koichi Sato, Keietsu Abe, Tadafumi Adschiri

    Journal of Materials Chemistry   22 ( 18 )   9041 - 9045   2012年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1039/c2jm30325f

    Web of Science

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  • Toll-like receptor 9-dependent activation of bone marrow-derived dendritic cells by URA5 DNA from <i>Cryptococcus neoformans</i>. 査読 国際誌

    Misuzu Tanaka, Keiko Ishii, Yuri Nakamura, Akiko Miyazato, Atsuko Maki, Yuzuru Abe, Tomomitsu Miyasaka, Hideki Yamamoto, Yukiko Akahori, Misaki Fue, Yurie Takahashi, Emi Kanno, Ryoko Maruyama, Kazuyoshi Kawakami

    Infection and immunity   80 ( 2 )   778 - 86   2012年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Cryptococcus neoformans is an opportunistic fungal pathogen that causes meningoencephalitis in immunocompromised patients. Recently, we reported that Toll-like receptor 9 (TLR9) is involved in host defense against C. neoformans: specifically, it detects the pathogen's DNA. In the present study, we aimed to elucidate the mechanisms underlying TLR9-mediated activation of innate immune responses by using the URA5 gene, which encodes a virulent component of this fungal pathogen. A PCR-amplified 345-bp URA5 gene fragment induced interleukin-12 p40 (IL-12p40) production by bone marrow-derived dendritic cells (BM-DCs) in a TLR9-dependent manner. Similar activity was detected in the 5' 129-bp DNA fragment of URA5 and in a synthesized oligodeoxynucleotide (ODN) with the same sequence. Shorter ODN fragments, which contained GTCGGT or GACGAT but had only 24 or 21 bases, induced IL-12p40 production and CD40 expression by BM-DCs, but this activity vanished when the CG sequence was replaced by GC or when a phosphorothioate modification was introduced. IL-12p40 production caused by active ODN was strikingly enhanced by treatment with DOTAP, a cationic lipid that increases the uptake of DNA by BM-DCs, though DOTAP failed to induce IL-12p40 production by inactive ODN and did not affect the activity of an ODN-containing canonical CpG motif. There was no apparent difference in intracellular trafficking between active and inactive ODNs. Finally, an extremely high dose of inactive ODN suppressed IL-12p40 production by BM-DCs that had been stimulated with active ODN. These results suggest that the C. neoformans URA5 gene activates BM-DCs through a TLR9-mediated signaling pathway, using a mechanism possibly independent of the canonical CpG motif.

    DOI: 10.1128/IAI.05570-11

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  • <i>Cryptococcus neoformans</i> suppresses the activation of bone marrow-derived dendritic cells stimulated with its own DNA, but not with DNA from other fungi. 査読 国際誌

    Hideki Yamamoto, Yuzuru Abe, Akiko Miyazato, Daiki Tanno, Misuzu Tanaka, Tomomitsu Miyasaka, Keiko Ishii, Kazuyoshi Kawakami

    FEMS immunology and medical microbiology   63 ( 3 )   363 - 72   2011年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DNA from Cryptococcus neoformans activates bone marrow-derived dendritic cells (BM-DCs) in a TLR9-dependent manner. In this study, we examined the effect of the culture supernatants of C. neoformans on the activation of BM-DCs caused by its own DNA. C. neoformans supernatants suppressed IL-12p40, IL-6 production and CD40 expression by BM-DCs stimulated with its own DNA, but not with CpG-ODN and DNA from Candida albicans, Saccharomyces cerevisiae or Escherichia coli. In a confocal microscopic analysis, C. neoformans DNA was colocalized with LAMP-1, a late endosomal marker, and TLR9. The culture supernatants did not show any apparent suppression of these responses. In a luciferase reporter assay, C. neoformans supernatants inhibited NFκB activation caused by its own DNA. These inhibitory activities were attenuated by treatment with heat or trypsin. These results indicate that C. neoformans secrete certain proteinous molecules that suppress the activation of BM-DCs caused by its own DNA.

    DOI: 10.1111/j.1574-695X.2011.00859.x

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書籍等出版物

  • 歯科衛生学辞典

    眞木, 吉信, 全国歯科衛生士教育協議会( 担当: 分担執筆 ,  範囲: 微生物学, 免疫学)

    2019年7月  ( ISBN:9784816013683

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    総ページ数:478p  

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MISC

  • クリプトコックス感染防御におけるClaudin欠損の影響

    佐藤光, 笠松純, 篠宮岳志, 山本秀輝, 石井恵子, 川上和義

    感染症学雑誌   95 ( 臨増 )   206 - 206   2021年4月

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    記述言語:日本語  

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  • クリプトコックス感染防御におけるClaudin欠損の影響

    佐藤光, 笠松純, 篠宮岳志, 山本秀輝, 石井恵子, 川上和義, 川上和義

    日本化学療法学会雑誌   69 ( Supplement-A )   2021年

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  • クリプトコックス感染防御におけるClaudins欠損の影響

    佐藤光, 笠松純, 山本秀輝, 石井恵子, 川上和義

    日本医真菌学会雑誌   61 ( suppl. )   81 - 81   2020年9月

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    記述言語:日本語   出版者・発行元:(一社)日本医真菌学会  

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  • クリプトコックス感染の自然免疫時相におけるメモリー、エフェクターT細胞からのIFN-γ産生

    中畑那奈, 梅木彩, 佐藤光, 笠松純, 山本秀輝, 石井恵子, 川上和義

    感染症学雑誌   94 ( 臨増 )   292 - 292   2020年3月

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    記述言語:日本語   出版者・発行元:(一社)日本感染症学会  

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  • クリプトコックス感染防御におけるTight junctionタンパク質欠損の影響

    佐藤光, 笠松純, 山本秀輝, 石井恵子, 川上和義

    感染症学雑誌   94 ( 臨増 )   292 - 292   2020年3月

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    記述言語:日本語   出版者・発行元:(一社)日本感染症学会  

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  • クリプトコックス感染におけるIL-17AによるTh1免疫応答の制御と防御機構への影響

    佐藤 光, 笠松 純, 山本 秀輝, 石井 恵子, 川上 和義

    日本医真菌学会雑誌   60 ( Suppl.1 )   87 - 87   2019年10月

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    記述言語:日本語   出版者・発行元:(一社)日本医真菌学会  

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  • クリプトコックス感染におけるIL-17Aを介したTh1免疫応答の制御と防御機構への影響

    佐藤 光, 山本 秀輝, 石井 恵子, 川上 和義

    感染症学雑誌   93 ( 臨増 )   323 - 323   2019年3月

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    記述言語:日本語   出版者・発行元:(一社)日本感染症学会  

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  • 真菌感染防御と糖鎖認識 C-type lectin receptorsによるクリプトコックスの認識と感染防御

    佐藤 光, 川上 和義, 中村 優里, 山本 秀輝, 丹野 大樹, 石井 恵子, 山崎 晶, 岩倉 洋一郎, 原 博満, 西城 忍

    Medical Mycology Journal   57 ( Suppl.1 )   76 - 76   2016年9月

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    記述言語:日本語   出版者・発行元:(一社)日本医真菌学会  

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  • クリプトコックス感染におけるTh1依存性防御応答のIL-17Aによる制御

    景澤 貴史, 野村 俊樹, 佐藤 光, 山本 秀輝, 松本 郁美, 横山 隣, 石井 恵子, 岩倉 洋一郎, 川上 和義

    感染症学雑誌   90 ( 臨増 )   329 - 329   2016年3月

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    記述言語:日本語   出版者・発行元:(一社)日本感染症学会  

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  • Cryptococcus neoformans感染免疫応答における1型インターフェロン受容体欠損の影響

    佐藤 光, 松村 香菜, 石井 恵子, 川上 和義, 山本 秀輝

    Medical Mycology Journal   54 ( Suppl.1 )   83 - 83   2013年9月

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    記述言語:日本語   出版者・発行元:(一社)日本医真菌学会  

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  • 免疫細胞のCryptococcus neoformans認識におけるC-type lectin receptorsの役割 Mincleを中心とした検討

    松村 香菜, 佐藤 光, 石井 恵子, 安達 禎之, 大野 尚仁, 川上 和義, 中村 優里, 山本 秀輝, 館 正弘, 山崎 晶, 原 博満

    Medical Mycology Journal   54 ( Suppl.1 )   83 - 83   2013年9月

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    記述言語:日本語   出版者・発行元:(一社)日本医真菌学会  

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  • Signaling via an adapter molecule CARD9 is essential for the host defense to infection with Cryptococcus neoformans

    Hideki Yamamoto, Yuri Nakamura, Yurie Takahashi, Ko Sato, Natsuo Yamamoto, Keiko Ishii, Hiromitsu Hara, Kazuyoshi Kawakami

    JOURNAL OF IMMUNOLOGY   188   2012年5月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Web of Science

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  • Earlier protective response and milder clinical course of Mycobacterium bovis BCG infection in mice lacking an adapter molecule CARD9

    Kazuyoshi Kawakami, Yurie Takahashi, Hideki Yamamoto, Yuri Nakamura, Keiko Ishii, Hiromitsu Hara

    JOURNAL OF IMMUNOLOGY   188   2012年5月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:AMER ASSOC IMMUNOLOGISTS  

    Web of Science

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  • クリプトコックス感染防御におけるdectin‐2及びCard9の役割

    中村優里, 山本秀輝, 高橋友里恵, 阿部譲, 石井恵子, 西城忍, 岩倉洋一郎, 原博満, 山崎晶, 川上和義

    日本生体防御学会学術総会講演抄録集   22nd   37   2011年

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    記述言語:日本語  

    J-GLOBAL

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講演・口頭発表等

  • The role of Dectin-2 and Mincle in the initiation of immune responses caused by influenza virus hemagglutinin

    Hideki Yamamoto, Chikako Tomiyama, Sho Yamasaki, Yoichiro Iwakura, Kazuyoshi Kawakami

    The 48th Annual Meeting of the Japanese Society for Immunology  2019年12月 

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    記述言語:英語   会議種別:ポスター発表  

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  • The role of C-type lectin receptor, Mincle in the recognition of influenza virus 国際会議

    Hideki Yamamoto, Chikako Tomiyama, Sho Yamasaki, Kazuyoshi Kawakami

    The 26th International Symposium on Molecular Cell Biology of Macrophages  2019年6月 

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    記述言語:英語   会議種別:ポスター発表  

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  • CARD9-mediated innate IFN-γ production and host defense to cryptococcal infection : involvement of memory phenotype T cells

    Hideki Yamamoto, Yuri Nakamura, Ko Sato, Kana Matsumura, Keiko Ishii, Hiromitsu Hara, Kazuyoshi Kawakami

    第42回日本免疫学会学術集会  2013年12月 

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    記述言語:英語   会議種別:口頭発表(一般)  

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  • Essential role of Card9 in innate IFN-γ production and Th17 differentiation in the host defense against cryptococcal infection. 国際会議

    Hideki Yamamoto, Yuri Nakamura, Ko Sato, Kana Matsumura, Natsuo Yamamoto, Keiko Ishii, Hiromitsu Hara, Kazuyoshi Kawakami

    The 28th International Congress of Chemotherapy and Infection  2013年6月 

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    記述言語:英語   会議種別:ポスター発表  

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  • Role of CARD9-mediated signaling in innate-phase IFN-γ production and Th17 differentiation in the host defense to cryptococcal infection

    Hideki Yamamoto, Yuri Nakamura, Ko Sato, Kana Matsumura, Natsuo Yamamoto, Keiko Ishii, Hiromitsu Hara, Kazuyoshi Kawakami

    第41回日本免疫学会学術集会  2012年12月 

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    記述言語:日本語   会議種別:口頭発表(一般)  

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  • Signaling via an adaptor molecule CARD9 is essential for the host defense to infection with Cryptococcus neoformans. 国際会議

    Hideki Yamamoto, Yuri Nakamura, Yurie Takahashi, Ko Sato, Natsuo Yamamoto, Keiko Ishii, Hiromitsu Hara, Kazuyoshi Kawakami

    The 99th American Association of Immunologist Annual Meeting  2012年5月 

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    記述言語:英語   会議種別:ポスター発表  

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  • Indispensable role of CARD9 in the host defense against infection with Cryptococcus neoformans

    Hideki Yamamoto, Yuri Nakamura, Yurie Takahashi, Natsuo Yamamoto, Keiko Ishii, Hiromitsu Hara, Kazuyoshi Kawakami

    第40回日本免疫学会学術集会  2011年11月 

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    記述言語:日本語   会議種別:口頭発表(一般)  

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  • Mycobacterium bovis BCG感染におけるCARD9遺伝子欠損の役割

    山本秀輝, 高橋友里恵, 中村優里, 石井恵子, 原博満, 川上和義

    第81回実験結核研究会  2011年5月 

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    記述言語:日本語   会議種別:口頭発表(一般)  

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  • Role of Dectin-2 and CARD9 in the activation of bone-marrow-derived dendritic cells by Mycobacterium bovis BCG. 国際会議

    Hideki Yamamoto, Natsuo Yamamoto, Misuzu Tanaka, Yurie Takahashi, Yuzuru Abe, Daiki Tanno, Tomomitsu Miyasaka, Keiko Ishii, Yoshiyuki Adachi, Naohito Ohno, Hiromitsu Hara, Shinobu Saijo, Yoichiro Iwakura, Kazuyoshi Kawakami

    The 14th International Congress of Immunology.  2010年8月 

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    記述言語:英語   会議種別:ポスター発表  

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  • クリプトコッカス感染防御におけるdectin-2及びCARD9の役割

    山本秀輝, 山本夏男, 田中三鈴, 高橋友里恵, 阿部譲, 石井恵子, 金光敬二, 川上和義

    第21回日本生体防御学会学術集会  2010年7月 

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    記述言語:日本語   会議種別:口頭発表(一般)  

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  • Dectin-2-dependent activation of myeloid dendritic cells stimulated with Cryptococcus neoformans and its role in the host defense.

    Hideki Yamamoto, Natsuo Yamamoto, Misuzu Tanaka, Akiko Miyazato, Yuzuru Abe, Daiki Tanno, Tetsuji Aoyagi, Keiko Ishii, Shinobu Saijo, Yoichiro Iwakura, Mitsuo Kaku, Kazuyoshi Kawakami

    第39回日本免疫学会総会・学術集会  2009年12月 

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    記述言語:日本語   会議種別:ポスター発表  

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  • クリプトコッカス培養上清によるTLR9を介した樹状細胞活性化に対する抑制活性

    山本秀輝, 阿部 譲, 田中三鈴, 丹野大樹, 石井恵子, 川上和義

    第20回日本生体防御学会学術集会  2009年7月 

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    記述言語:日本語   会議種別:口頭発表(一般)  

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▶ 全件表示

共同研究・競争的資金等の研究

  • 新規インフルエンザワクチンアジュバント開発を目指したC型レクチン受容体の機能解明

    研究課題/領域番号:20K17461  2020年4月 - 2022年3月

    日本学術振興会  科学研究費助成事業 若手研究  若手研究

    山本 秀輝

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    担当区分:研究代表者 

    配分額:4160000円 ( 直接経費:3200000円 、 間接経費:960000円 )

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  • インフルエンザワクチンにおける新規アジュバント探索に向けたC型レクチン受容体の機能解析

    2019年 - 2022年

    武田科学振興財団  2019年度医学系研究助成(感染領域) 

    山本 秀輝

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    担当区分:研究代表者  資金種別:競争的資金

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  • インフルエンザ誘発ARDSの新規制御機序確立に向けたC型レクチン受容体の機能解析

    研究課題/領域番号:18K16510  2018年4月 - 2020年3月

    日本学術振興会  科学研究費助成事業 若手研究  若手研究

    山本 秀輝

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    担当区分:研究代表者 

    配分額:4160000円 ( 直接経費:3200000円 、 間接経費:960000円 )

    本研究は、微生物多糖を認識するパターン認識受容体であるC型レクチン受容体(CLRs)が、インフルエンザにより誘発される急性呼吸促迫症候群(ARDS)の発症病態にどう関与しているのかを解明することを目的としている。このCLRsのうち、本研究では高マンノース多糖を認識するDectin-2およびMincleに着目して、インフルエンザウイルス(IFV)とCLRsの相互作用について解析を行った。
    (1)第1に、Dectin-2またはMincleにリガンドが結合しシグナルが伝達されると、転写因子NFATが緑色蛍光タンパク(GFP)を発現させるレポーター細胞を、IFV膜表面主要抗原であるヘマグルチニン(HA)で刺激した。A型株であるH1N1株およびH3N2株由来HA刺激により、Mincle発現細胞でGFP発現がみられた。また、B型株であるビクトリア系統株および山形系統株由来HA刺激でも、A型株と同様のGFP発現が観察された。一方でDectin-2は、H3N2株由来HA刺激でGFP発現が観察されたが、その他の株由来HA刺激では、わずかなGFP発現に留まった。
    (2)第2に、骨髄由来樹状細胞をIFV由来HAで24時間刺激することで産生される炎症性サイトカイン量をELISAにて測定し、炎症誘導への関与を評価した。B型株由来HA刺激によるサイトカイン産生は、A型株と比較して優位であった。さらに、両株のHA刺激により産生されるIL-12p40およびIL-6産生は、野生型マウスと比較してDectin-2遺伝子欠損(KO)マウスにおいて有意に低下した。一方で、Mincle KOマウスにおけるIL-12p40およびIL-6産生は、野生型マウスと同等であった。
    以上の結果から、IFVの認識および炎症反応誘導において、Dectin-2が重要な役割を果たしている可能性が示唆された。

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  • インフルエンザ重症化制御に向けた宿主免疫応答の解明 -C型レクチン受容体に着目して‐

    2018年 - 2019年

    花王健康科学研究会  第16回花王健康科学研究会研究助成 

    山本 秀輝

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    担当区分:研究代表者  資金種別:競争的資金

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  • 糖脂質抗原を用いた新たな真菌ワクチンの開発

    研究課題/領域番号:17K19642  2017年6月 - 2019年3月

    日本学術振興会  科学研究費助成事業 挑戦的研究(萌芽)  挑戦的研究(萌芽)

    川上和義, 山本秀輝

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    担当区分:研究分担者 

    配分額:6370000円 ( 直接経費:4900000円 、 間接経費:1470000円 )

    Cryptococcus neoformansは、エイズなど免疫不全患者に重症の髄膜炎を引き起こすことで臨床において問題となっている。本研究では、C. neoformanに対するワクチン開発を目的として、マウスモデルでのβ-glucosylceramide(β-GlcCer)による抗体産生効果及び有効なアジュバントの探索を実施した。β-GlcCerを非メチル化CpGオリゴDNAとともに投与することで、血清中に特異的IgM、IgG抗体が産生された。さらに、免疫細胞によるβ-GlcCerの認識及び感染初期の炎症反応制御へのMincleの関与を示唆する結果が得られた。

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担当経験のある授業科目

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    機関名:新潟大学

  • 基礎免疫学

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    機関名:新潟大学

  • 医学検査管理総論

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  • 病態化学分析学Ⅱ

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    機関名:新潟大学

  • 医学検査機器概論

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    現在
    機関名:新潟大学

  • スタディスキルズ (検査)

    2019年
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    機関名:新潟大学

  • 分析系検査管理論

    2019年
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    機関名:新潟大学

  • 卒業研究

    2019年
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    機関名:新潟大学

  • 病態化学分析学Ⅰ

    2019年
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    現在
    機関名:新潟大学

  • 免疫検査科学

    2019年
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    機関名:新潟大学

  • 免疫検査学演習

    2018年
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    現在
    機関名:新潟大学

  • 免疫検査科学実習

    2018年
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    機関名:新潟大学

  • 医療英語(検査)

    2018年
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    2019年
    機関名:新潟大学

  • 微生物検査科学演習

    2018年
    機関名:新潟大学

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