Updated on 2024/11/10

写真a

 
YAMAMOTO Hideki
 
Organization
Academic Assembly Institute of Medicine and Dentistry Health Sciences Assistant Professor
Faculty of Medicine School of Health Sciences Assistant Professor
Title
Assistant Professor
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Degree

  • 博士(保健学) ( 2014.3   東北大学 )

Research Interests

  • 生体防御学

  • 真菌

  • インフルエンザ

Research Areas

  • Life Science / Emergency medicine

  • Life Science / Immunology

  • Life Science / Infectious disease medicine

Research History (researchmap)

  • Niigata University   Assistant Professor

    2021.4

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    Country:Japan

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  • Niigata University   Center for Transdisciplinary Research, Institute of Research Promotion   Assistant Professor

    2020.4 - 2021.3

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    Country:Japan

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  • Niigata University   Center for Transdisciplinary Research, Institute of Research Promotion   Specially Appointed Assistant Professor

    2017.1 - 2020.3

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  • 東北大学大学院医学系研究科医科学専攻   整形外科学分野

    2014.4 - 2016.12

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  • 東北大学大学院医学系研究科保健学専攻   博士後期課程

    2011.4 - 2014.3

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  • 東北大学大学院医学系研究科保健学専攻   博士前期課程

    2009.4 - 2011.3

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Research History

  • Niigata University   Health Sciences, Institute of Medicine and Dentistry, Academic Assembly   Assistant Professor

    2021.4

  • Niigata University   Institute for Research Promotion Center for Transdisciplinary Research   Assistant Professor

    2020.4 - 2021.3

  • Niigata University   Institute for Research Promotion Center for Transdisciplinary Research   Specially Appointed Assistant Professor

    2017.1 - 2020.3

Education

  • Tohoku University   Graduate School of Medicine   保健学専攻 博士後期課程 修了

    - 2014.3

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    Country: Japan

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Professional Memberships

Qualification acquired

  • Medical Technologist

 

Papers

  • Innate phase production of IFN-γ by memory and effector T cells expressing early activation marker CD69 during infection with Cryptococcus deneoformans in the lungs. Reviewed International journal

    Anna Miyahara, Aya Umeki, Ko Sato, Toshiki Nomura, Hideki Yamamoto, Tomomitsu Miyasaka, Daiki Tanno, Ikumi Matsumoto, Tong Zong, Takafumi Kagesawa, Akiho Oniyama, Kotone Kawamura, Xiaoliang Yuan, Rin Yokoyama, Yuki Kitai, Emi Kanno, Hiromasa Tanno, Hiromitsu Hara, Sho Yamasaki, Shinobu Saijo, Yoichiro Iwakura, Keiko Ishii, Kazuyoshi Kawakami

    Infection and immunity   e0002424   2024.5

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    Language:English   Publishing type:Research paper (scientific journal)  

    Cryptococcus deneoformans is a yeast-type fungus that causes fatal meningoencephalitis in immunocompromised patients and evades phagocytic cell elimination through an escape mechanism. Memory T (Tm) cells play a central role in preventing the reactivation of this fungal pathogen. Among these cells, tissue-resident memory T (TRM) cells quickly respond to locally invaded pathogens. This study analyzes the kinetics of effector T (Teff) cells and Tm cells in the lungs after cryptococcal infection. Emphasis is placed on the kinetics and cytokine expression of TRM cells in the early phase of infection. CD4+ Tm cells exhibited a rapid increase by day 3, peaked at day 7, and then either maintained their levels or exhibited a slight decrease until day 56. In contrast, CD8+ Tm cells reached their peak on day 3 and thereafter decreased up to day 56 post-infection. These Tm cells were predominantly composed of CD69+ TRM cells and CD69+ CD103+ TRM cells. Disruption of the CARD9 gene resulted in reduced accumulation of these TRM cells and diminished interferon (IFN) -γ expression in TRM cells. TRM cells were derived from T cells with T cell receptors non-specific to ovalbumin in OT-II mice during cryptococcal infection. In addition, TRM cells exhibited varied behavior in different tissues. These results underscore the importance of T cells, which produce IFN-γ in the lungs during the early stage of infection, in providing early protection against cryptococcal infection through CARD9 signaling.

    DOI: 10.1128/iai.00024-24

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  • Involvement of Dectin-2 in the innate inflammatory response triggered by influenza virus hemagglutinin Reviewed

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

    Advances in Infectious Diseases   13 ( 3 )   478 - 497   2023.9

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    Authorship:Lead author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.4236/aid.2023.133039

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

    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   2021.12

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher: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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    Other Link: https://www.nature.com/articles/s41598-021-00708-6

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

    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   2021.4

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    Authorship:Lead author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher: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 Reviewed

    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   2021.4

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher: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 Reviewed

    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   2020.12

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher: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> Reviewed International journal

    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   2020.10

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher: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>. Reviewed International journal

    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   2020.8

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    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 Reviewed

    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   2020.6

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    DOI: 10.1159/000508535

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  • Dectin-2-mediated signaling triggered by the cell wall polysaccharides of <i>Cryptococcus neoformans</i>. Reviewed International journal

    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   2019.12

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    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 Reviewed

    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

    Journal of Health Sciences of Niigata University   16 ( 1 )   1 - 10   2019.5

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  • Contribution of CARD9-mediated signalling to wound healing in skin Reviewed International journal

    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   2017.11

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    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 Reviewed

    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   2017.9

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    The wound-healing process consists of the inflammation, proliferation, and remodeling phases. In chronic wounds, the inflammation phase is prolonged with persistent neutrophil infiltration. The inflammatory response is critically regulated by cytokines and chemokines that are secreted from various immune cells. Recently, we showed that skin wound healing was delayed and the healing process was impaired under conditions lacking invariant natural killer T (iNKT) cells, an innate immune lymphocyte with potent immuno-regulatory activity. In the present study, we investigated the effect of iNKT cell deficiency on the neutrophilic inflammatory response during the wound healing process. Neutrophil infiltration was prolonged in wound tissue in mice genetically lacking iNKT cells (Jα18KO mice) than in wild-type (WT) control mice on days 1 and 3 after wounding. MIP-2, KC, and IL-17A were produced at a significantly higher level in Jα18KO mice than in WT mice. In addition, neutrophil apoptosis was significantly reduced in the wound tissue in Jα18KO mice than in WT mice. Treatment with anti-IL-17A mAb, anti-Gr-1 mAb, or neutrophil elastase inhibitor reversed the impaired wound healing in Jα18KO mice. These results suggest that iNKT cells may promote the wound healing process through preventing the prolonged inflammatory response mediated by neutrophils.

    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 Reviewed

    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   2015.9

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    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>. Reviewed International journal

    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   2015.2

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    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>. Reviewed International journal

    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   2014.4

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    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-1<SUP>dull+</SUP> Cells in the Production of TNF-α and IL-17 and Exacerbated Systemic Inflammatory Response Caused by Lipopolysaccharide Reviewed

    Hideki Yamamoto

    Inflammation   37 ( 1 )   186 - 195   2014.2

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    DOI: 10.1007/S10753-013-9729-5

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    Other Link: 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 Reviewed

    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   2013.8

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    DOI: 10.1111/cei.12106

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

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

    Journal of Materials Chemistry   22 ( 18 )   9041 - 9045   2012.5

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    In our study, water dispersible magnetite (Fe3O4) nanoparticles were continuously synthesized in water under high temperature and pressure in the presence of 3,4-dihydroxyhydrocinnamic acid (DHCA) by using a tubular flow reactor. The prepared Fe3O4 nanoparticles were well dispersed in water because the surfaces of the nanoparticles were fully covered by DHCA molecules and the -COOH groups in the DHCA molecules were exposed to the surrounding water. Cytokines such as IL-12 and TNF-alpha were not produced from the dendritic cells of mice by co-incubation with our synthesized Fe3O4. This indicates that the synthesized Fe3O4 had no immune stimulating property for the dendritic cells of the mouse. Therefore, our synthesized Fe3O4 nanoparticles are suitable for biological applications such as magnetic resonance imaging contrast agents and carriers for drug and gene delivery, and in areas such as hyperthermia therapy for cancer, biosensors, and tissue engineering.

    DOI: 10.1039/c2jm30325f

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

    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   2012.2

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    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. Reviewed International journal

    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   2011.12

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    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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Books

  • 歯科衛生学辞典

    ( Role: Contributor)

    永末書店  2019.7  ( ISBN:9784816013683

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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   2021.4

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    Language:Japanese   Publisher:(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

  • 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   2020.9

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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   2020.3

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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   2020.3

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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   2019.10

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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   2019.3

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  • Candida glabrata細胞壁糖鎖合成酵素遺伝子欠損株alg6Δ及びmnn2Δの性質

    伊藤 文恵, 高橋 静香, 田中 大, 工藤 敦, 佐々木 雅人, 岡本 美智代, 高橋 梓, 山口 正規, 山本 秀輝, 丹野 大樹, 横山 隣, 川上 和義, 知花 博治, 柴田 信之

    日本薬学会年会要旨集   137年会 ( 3 )   186 - 186   2017.3

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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   2016.9

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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   2016.3

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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   2013.9

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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   2013.9

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    CiNii Article

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  • Essential role of Card9 in innate IFN-gamma production and Th17 differentiation in the host defense against cryptococcal infection

    H. Yamamoto, Y. Nakamura, K. Sato, K. Matsumura, N. Yamamoto, K. Ishii, H. Hara, K. Kawakami

    INTERNATIONAL JOURNAL OF ANTIMICROBIAL AGENTS   42   S126 - S126   2013.6

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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   2012.5

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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   2012.5

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  • 免疫回避機能を有する医療用水溶性磁性ナノ粒子の連続合成

    冨樫貴成, 高見誠一, 川上和義, 山本秀輝, 名嘉節, 佐藤康一, 阿尻雅文

    ナノ学会大会講演予稿集   10th   2012

  • 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

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    J-GLOBAL

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  • 常在微生物による肺炎及び血流感染に対するIL-13の宿主保護的な役割

    山本夏男, 三浦里織, 高橋実, 藤田禎三, 大花昇, 今福裕司, 細川裕之, 中山俊憲, 山本秀輝, 川上和義, 賀来満夫, 金光敬二

    日本生体防御学会学術総会講演抄録集   22nd   2011

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Presentations

  • 樹状細胞の自然炎症に寄与するA群溶連菌由来タンパク及び生体由来因子の解析

    山本夏男, 鈴木剛, 山本秀輝, 大宮卓, 勝見正道, 西村秀一, 伊関憲

    第76回日本細菌学会東北支部総会  2024.8 

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  • 血流感染時の生存期間に寄与するIgM抗体の量と質をIL-13が調整する:type-1型自然炎症との比較

    山本 夏男, 鈴木 剛, 原 靖果, 仲村 究, 山本 秀輝, 金光 敬二

    第98回日本感染症学会学術講演会/第72回日本化学療法学会総会 合同学会  2024.6 

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  • 腹膜炎急性期の自然免疫応答で生じる心臓障害と抗炎症サイトカインIL-13の関与

    鈴木剛, 山本秀輝, 金光敬二, 山本夏男

    第98回日本感染症学会学術講演会/第72回日本化学療法学会総会 合同学会  2024.6 

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  • 血流感染で莢膜保有肺炎球菌を中和するIgM抗体の量と質をIL-13が調整する:臓器内type-1型自然炎症との比較

    山本 夏男, 鈴木 剛, 山本 秀輝, 原 靖果, 仲村 究, 金光 敬二

    第72回日本感染症学会東日本地方会学術集会/第70回日本化学療法学会東日本支部総会 合同学会  2023.10 

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    Event date: 2023.10

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  • 腹膜炎急性期の自然免疫応答で生じる臓器障害に関わるIL-13とCタイプレクチンの役割

    鈴木 剛, 山本 秀輝, 金光 敬二, 山本 夏男

    第72回日本感染症学会東日本地方会学術集会/第70回日本化学療法学会東日本支部総会 合同学会  2023.10 

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  • Involvement of Dectin-2 in the initiation of innate immune response triggered by influenza virus hemagglutinin

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

    The 87th Annual Meeting of the Japanese Society of Interferon and Cytokine Research/The 29th International Symposium on Molecular Cell Biology of Macrophages Joint Symposium  2023.5 

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    Event date: 2023.5

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  • Involvement of Dectin-2 in the host recognition and specific antibody response triggered by influenza virus hemagglutinin.

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

    The 50th Annual Meeting of the Japanese Society for Immunology  2021.12 

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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

    第95回日本感染症学会総会・学術講演会  2021.5 

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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

    第64回日本医真菌学会総会・学術集会  2020.10 

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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

    第94回日本感染症学会総会・学術講演会  2020.8 

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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

    第94回日本感染症学会総会・学術講演会  2020.8 

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  • 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  2019.12 

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  • Relationship between dendritic cell modulation and autoimmune hepatitis exacerbation during high fat feeding

    Chikako Tomiyama, Hideki Yamamoto, Hisami Watanabe

    The 48th Annual Meeting of the Japanese Society for Immunology  2019.12 

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  • クリプトコックス感染の自然免疫相におけるIFN-γ産生機構の解析

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

    第68回日本感染症学会東日本学術集会・第68回日本化学療法学会東日本支部総会  2019.10 

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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

    第63回日本医真菌学会総会・学術集会  2019.10 

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  • クリプトコックス感染におけるIL-17Aによる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

    第73回日本細菌学会東北支部総会  2019.8 

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  • The role of C-type lectin receptor, Mincle in the recognition of influenza virus International conference

    Hideki Yamamoto, Chikako Tomiyama, Sho Yamasaki, Kazuyoshi Kawakami

    The 26th International Symposium on Molecular Cell Biology of Macrophages  2019.6 

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  • Exacerbation mechanisms of autoimmune hepatitis in the low estrogen status and its relationship with hepatic dendritic cells

    Chikako Tomiyama, Hiroki Hirama, Hideki Yamamoto, Hisami Watanabe

    The 26th International Symposium on Molecular Cell Biology of Macrophages  2019.6 

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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

    第93回日本感染症学会総会・学術講演会  2019.4 

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  • Possible factors which exacerbate autoimmune hepatitis in low-level estrogen

    Hiroki Hirama, Chikako Tomiyama, Hisami Watanabe, Hideki Yamamoto

    The 47th Annual Meeting of the Japanese Society for Immunology  2018.12 

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  • インターロイキン17によるクリプトコックス感染免疫応答の制御

    佐藤光, 笠松純, 山本秀輝, 石井恵子, 川上和義

    第2回東北医真菌研究会  2018.12 

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  • Candida glabrata細胞壁糖鎖合成酵素遺伝子欠損株alg6Δ及びmnn2Δの性質

    伊藤 文恵, 高橋 静香, 田中 大, 工藤 敦, 佐々木 雅人, 岡本 美智代, 高橋 梓, 山口 正視, 山本 秀輝, 丹野 大樹, 横山 隣, 川上 和義, 知花 博治, 柴田 信之

    日本薬学会第137年会  2017.3 

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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

    第90回日本感染症学会総会・学術講演会  2016.4 

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  • Accumulation of tissue resident memory T cells expressing IFN-γ in lungs during infection with Cryptococcus neoformans

    Anna Miyahara, Toshiki Nomura, Hideki Yamamoto, Ko Sato, Keiko Ishii, Ikumi Matsumoto, Tong Zong, Takafumi Kagesawa, Hiromitsu Hara, Kazuyoshi Kawakami

    The 44th Annual Meeting of the Japanese Society for Immunology  2015.11 

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  • クリプトコックス感染防御におけるIL-17A の役割

    野村俊樹, 佐藤光, 山本秀輝, 松本郁美, 石井恵子, 岩倉洋一郎, 川上和義

    第25回日本生体防御学会学術総会  2014.7 

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  • クリプトコックス感染防御における1 型インターフェロンの役割

    松本郁美, 佐藤光, 山本秀輝, 野村俊樹, 石井恵子, 宇野賀津子, 川上和義

    第25回日本生体防御学会学術総会  2014.7 

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  • 真菌感染におけるⅠ型インターフェロンの産生と感染防御における役割

    佐藤光, 山本秀輝, 野村俊樹, 石井恵子, 川上和義

    第33回東北免疫研究会  2014.3 

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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  2013.12 

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  • Defect of type Ⅰ interferon receptor leads to improved infection with Cryptococcus neoformans in parallel to increased production in IFN-γ and MAC5AC in lungs

    Ko Sato, Hideki Yamamoto, Keiko Ishii, Kazuyoshi Kawakami

    The 42th Annual Meeting of the Japanese Society for Immunology  2013.12 

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  • I型インターフェロン受容体欠損マウスにおけるCryptococcus neoformansの排除とムチン産生の亢進

    佐藤光, 山本秀輝, 石井恵子, 川上和義

    第67回日本細菌学会東北支部総会  2013.8 

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  • Cryptococcus neoformansとC-type lectin receptorとの相互作用

    松村香菜, 中村優里, 山本秀輝, 佐藤光, 石井恵子, 山崎晶, 原博満, 安達禎之, 大野尚仁, 館正弘, 川上和義

    第24回日本生体防御学会学術総会  2013.7 

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  • Cryptococcus neoformans感染防御におけるtype Ⅰ interferonの役割

    佐藤光, 山本秀輝, 石井恵子, 川上和義

    第24回日本生体防御学会学術総会  2013.7 

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

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

    The 28th International Congress of Chemotherapy and Infection  2013.6 

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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

    2012.12 

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  • Immune adjuvant activity of oligonucleotide DNA from Cryptococcus neoformans

    Ko Sato, Yuri Nakamura, Hideki Yamamoto, Keiko Ishii, Kazuyoshi Kawakami

    The 41th Annual Meeting of the Japanese Society for Immunology  2012.12 

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  • Effect of Dectin-2 deficiency on the host inflammatory response during infection with Cryptococcus neoformans

    Kana Matsumura, Hideki Yamamoto, Yuri Nakamura, Ko Sato, Keiko Ishii, Shinobu Saijo, Yoichiro Iwakura, Kazuyoshi Kawakami

    The 41th Annual Meeting of the Japanese Society for Immunology  2012.12 

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  • Memory T cells response after infection with Cryptococcus neoformans in mice

    Yuri Nakamura, Ko Sato, Hideki Yamamoto, Keiko Ishii, Kazuyoshi Kawakami

    The 41th Annual Meeting of the Japanese Society for Immunology  2012.12 

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  • クリプトコックス感染初期のIFN-γ産生におけるCARD9 の役割とメモリーフェノタイプT 細胞の関与

    佐藤光, 山本秀輝, 中村優里, 高橋友里恵, 松村香菜, 石井恵子, 原博満, 館正弘, 川上和義

    第66回日本細菌学会東北支部総会  2012.8 

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  • Cryptococcus neoformans DNAによるマウス骨髄由来樹状細胞活性化とアジュバント活性

    中村優里, 石井恵子, 山本秀輝, 佐藤光, 松村香菜, 館正弘, 川上和義

    第23回日本生体防御学会学術総会  2012.7 

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  • CARD9欠損によるクリプトコックス感染の増悪機序

    佐藤光, 山本秀輝, 中村優里, 石井恵子, 松村香菜, 館正弘, 原博満, 川上和義

    第23回日本生体防御学会学術総会  2012.7 

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  • 免疫回避能を有する医療用磁性ナノ粒子の連続合成

    冨樫貴成, 高見誠一, 川上和義, 山本秀輝, 名嘉節, 佐藤康一, 阿尻雅文

    ナノ学会第10回大会  2012.6 

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  • Signaling via an adaptor molecule CARD9 is essential for the host defense to infection with Cryptococcus neoformans. International conference

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

    The 99th American Association of Immunologist Annual Meeting  2012.5 

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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

    2011.11 

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  • Limited role of Dectin-2 in the host defense to infection with Cryptococcus neoformans

    Yuri Nakamura, Hideki Yamamoto, Yurie Takahashi, Keiko Ishii, Yoshiyuki Adachi, Naohito Ohno, Shinobu Saijo, Yoichiro Iwakura, Hiromitsu Hara, Sho Yamasaki, Kazuyoshi Kawakami

    The 40th Annual Meeting of the Japanese Society for Immunology  2011.11 

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  • Mycobacterium bovis BCGにおけるCard9遺伝子欠損の影響

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

    The 40th Annual Meeting of the Japanese Society for Immunology  2011.11 

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  • 流通式水熱反応装置を用いた医療用磁性ナノ材料の連続合成と免疫反応評価

    冨樫貴成, 高見誠一, 川上和義, 山本秀輝, 名嘉節, 佐藤康一, 阿部敬悦, 阿尻雅文

    化学工学会第43回秋季大会  2011.9 

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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

    第22回日本生体防御学会学術総会  2011.6 

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  • Mycobacterium bovis BCGにおけるCard9遺伝子欠損の影響

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

    第22回日本生体防御学会学術総会  2011.6 

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  • クリプトコックスによるNKT細胞活性化とパターン認識下流分子の役割

    笛未崎, 阿部譲, 山本秀輝, 原博満, 石井恵子, 川上和義

    第22回日本生体防御学会学術総会  2011.6 

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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  2011.5 

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

    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.  2010.8 

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  • Depletion of Gr-1+ cells leads to the lethal systemic inflammatory responsesyndrome with multi-organ failure in mice

    Kazuyoshi Kawakami, Daiki Tanno, Tetsuji Aoyagi, Natsuo Yamamoto, Yuzuru Abe, Misuzu Tanaka, Tomomitsu Miyasaka, Hideki Yamamoto, Keiko Ishii, Hiroyuki Kunishima, Yoichi Hirakata, Mitsuo Kaku

    The 14th International Congress of Immunology  2010.8 

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  • LR9-dependent activation of bone marrow-derived dendritic cells by URA5 DNA from Cryptococcus neoformans

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

    The 14th International Congress of Immunology  2010.8 

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  • Role for dectin-2 and CARD9 in the host immune response to Cryptococcus neoformans

    Natsuo Yamamoto, Akiko Miyazato, Hideki Yamamoto, Yuzuru Abe, Misuzu Tanaka, Daiki Tanno, Tomomitsu Miyasaka, Keiko Ishii, Shinobu Saijo, Yoishiro Iwakura, Hiromitsu Hara, Kazuyoshi Kawakami

    The 14th International Congress of Immunology  2010.8 

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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  2010.7 

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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

    The 39th Annual Meeting of the Japanese Society for Immunology  2009.12 

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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総会  2009.7 

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Research Projects

  • Elucidation of the influenza prevention mechanisms by targeting glycan recognition receptors

    Grant number:22K08577

    2022.4 - 2025.3

    System name:Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (C)

    Research category:Grant-in-Aid for Scientific Research (C)

    Awarding organization:Japan Society for the Promotion of Science

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    Grant amount:\4160000 ( Direct Cost: \3200000 、 Indirect Cost:\960000 )

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  • Elucidation of the function of C-type lectin receptors for the development of novel influenza vaccine adjuvant

    Grant number:20K17461

    2020.4 - 2022.3

    System name:Grants-in-Aid for Scientific Research Grant-in-Aid for Early-Career Scientists

    Research category:Grant-in-Aid for Early-Career Scientists

    Awarding organization:Japan Society for the Promotion of Science

    Yamamoto Hideki

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    Grant amount:\4160000 ( Direct Cost: \3200000 、 Indirect Cost:\960000 )

    In the present study, we investigated whether influenza virus hemagglutinin (HA) is involved in the initiation of inflammatory responses, particularly of HA-specific antibody responses, induced by C-type lectin receptors. Each HA, especially HA derived from A/H3N2 subtype, was bound to murine or human Dectin-2 carbohydrate domain. Total IgG titer was significantly increased in Dectin-2 gene-deficient mice compared to wild-type mice upon intraperitoneal administration with HA derived from A/H3N2 subtype. These results suggested that Dectin-2 recognizes influenza virus HA and may be involved in some mechanism that further affects HA-specific antibody production.

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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 - 2022

    System name:2019年度医学系研究助成(感染領域)

    Awarding organization:武田科学振興財団

    山本 秀輝

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  • Basic study in the role of C-type lectin receptors to develop novel regulating system of acute respiratory distress syndrome caused by influenza infection.

    Grant number:18K16510

    2018.4 - 2020.3

    System name:Grants-in-Aid for Scientific Research Grant-in-Aid for Early-Career Scientists

    Research category:Grant-in-Aid for Early-Career Scientists

    Awarding organization:Japan Society for the Promotion of Science

    Yamamoto Hideki

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    Grant amount:\4160000 ( Direct Cost: \3200000 、 Indirect Cost:\960000 )

    The function of C-type lectin receptors (CLRs), known as pathogen-derived carbohydrate recognition receptors, in influenza infection has not been fully understood. Inflammatory cytokine production by bone marrow-derived dendritic cells upon stimulation with various types of influenza virus hemagglutinin (HA) was significantly reduced in Dectin-2 knockout mice compared to wild type mice. This reduction was closely related to the interaction between HA including high mannose polysaccharide and Dectin-2. The present studies suggested that Dectin-2 may play an important role for regulating severe influenza pneumoniae such as acute respiratory distress syndrome.

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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 - 2019

    System name:第16回花王健康科学研究会研究助成

    Awarding organization:花王健康科学研究会

    山本 秀輝

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  • Development of a novel fungal vaccine with glycolipid antigens

    Grant number:17K19642

    2017.6 - 2019.3

    System name:Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Research (Exploratory)

    Research category:Grant-in-Aid for Challenging Research (Exploratory)

    Awarding organization:Japan Society for the Promotion of Science

    Kawakami Kazuyoshi

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    Authorship:Coinvestigator(s) 

    Grant amount:\6370000 ( Direct Cost: \4900000 、 Indirect Cost:\1470000 )

    Cryptococcus neoformans causes fatal meningitis in immunocompromised patients, such as AIDS. In this study, to develop anti-fungal vaccines against C. neoformans infection, we addressed the ability of β-glucosylceramide (β-GlcCer) to induce the specific antibody and explored the effective adjuvants for this vaccine using a mouse model. Administration of β-GlcCer together with unmethylated CpG containing oligo DNA, a TLR9 ligand, led to increase in the serum level of IgM and IgG antibody against β-GlcCer. In NFAT-GFP reporter cells expressing Mincle, β-GlcCer induced GFP expression, suggesting the possible involvement of Mincle in the immune recognition of this glycolipid. In addition, we obtained the results suggesting the involvement of this pattern recognition receptor in the regulation of inflammatory responses caused by C. neoformans infection.

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Teaching Experience (researchmap)

  • Laboratory and Pathophysiological Immunology

    2023.4

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  • Practice of Laboratory and Pathophysiological Immunology

    2023.4

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  • Clinical Aspect of Laboratory Human Sciences

    2023.4

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  • History of Medicine and Health Care

    2022.4

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  • Acurracy Management of Laboratory Medicine

    2021

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  • Medical English Basic

    2021

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  • Clinical Chemical Analysis II

    2019

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  • Basic Immunology

    2019

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  • Study Skills

    2019

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  • Clinical Immunology

    2019

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  • Medical Quality and Safety Science

    2019

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  • Clinical Microbiology Laboratory

    2019

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  • Basic Understanding of Analytical Instruments in Medical Lab

    2019

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  • Comprehensive health sciences

    2018

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  • Clinical Immunology Practice

    2018

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  • Laboratory of Clinical Immunology

    2018

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  • Graduation Thesis

    2018

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  • Medical English

    2018

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Teaching Experience

  • 免疫・血液病態検査科学特講演習

    2024
    Institution name:新潟大学

  • 免疫・血液病態検査科学特講

    2024
    Institution name:新潟大学

  • 医学と医療の歴史

    2023
    Institution name:新潟大学

  • 免疫病態検査学特論

    2023
    Institution name:新潟大学

  • 臨床生体情報検査科学論

    2023
    Institution name:新潟大学

  • 免疫病態検査学実習

    2023
    Institution name:新潟大学

  • 医学検査管理総論

    2022
    Institution name:新潟大学

  • 臨床検査実習

    2022
    Institution name:新潟大学

  • 医療英語(検査)

    2022
    Institution name:新潟大学

  • 保健学総合

    2021
    Institution name:新潟大学

  • 医療安全管理学

    2020
    Institution name:新潟大学

  • 基礎免疫学

    2020
    Institution name:新潟大学

  • 医学検査機器概論

    2020
    Institution name:新潟大学

  • 病態化学分析学Ⅱ

    2020
    -
    2021
    Institution name:新潟大学

  • 医学検査管理総論

    2020
    Institution name:新潟大学

  • スタディスキルズ (検査)

    2019
    Institution name:新潟大学

  • 分析系検査管理論

    2019
    Institution name:新潟大学

  • 卒業研究

    2019
    Institution name:新潟大学

  • 病態化学分析学Ⅰ

    2019
    Institution name:新潟大学

  • 免疫検査科学

    2019
    Institution name:新潟大学

  • 免疫検査学演習

    2018
    Institution name:新潟大学

  • 免疫検査科学実習

    2018
    Institution name:新潟大学

  • 医療英語(検査)

    2018
    -
    2019
    Institution name:新潟大学

  • 微生物検査科学演習

    2018
    Institution name:新潟大学

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