2021/10/25 更新

写真a

カンダ ヤスヒロ
神田 泰洋
KANDA Yasuhiro
所属
教育研究院 医歯学系 医学系列 助教
医学部 医学科 助教
医歯学総合研究科 地域疾病制御医学専攻 助教
職名
助教
外部リンク

学位

  • 博士(医学) ( 2010年12月   新潟大学 )

研究分野

  • ライフサイエンス / 免疫学

  • ライフサイエンス / 寄生虫学

経歴(researchmap)

  • 新潟大学   医学部   助教

    2006年4月 - 現在

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経歴

  • 新潟大学   医学部 医学科   助教

    2006年4月 - 現在

  • 新潟大学   医歯学総合研究科 地域疾病制御医学専攻   助教

    2006年4月 - 現在

所属学協会

 

論文

  • Motility Dynamics of T Cells in Tumor-Draining Lymph Nodes: A Rational Indicator of Antitumor Response and Immune Checkpoint Blockade 招待 査読

    Yasuhiro Kanda, Taku Okazaki, Tomoya Katakai

    Cancers   13 ( 18 )   4616 - 4616   2021年9月

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    担当区分:筆頭著者   掲載種別:研究論文(学術雑誌)   出版者・発行元:MDPI AG  

    The migration status of T cells within the densely packed tissue environment of lymph nodes reflects the ongoing activation state of adaptive immune responses. Upon encountering antigen-presenting dendritic cells, actively migrating T cells that are specific to cognate antigens slow down and are eventually arrested on dendritic cells to form immunological synapses. This dynamic transition of T cell motility is a fundamental strategy for the efficient scanning of antigens, followed by obtaining the adequate activation signals. After receiving antigenic stimuli, T cells begin to proliferate, and the expression of immunoregulatory receptors (such as CTLA-4 and PD-1) is induced on their surface. Recent findings have revealed that these ‘immune checkpoint’ molecules control the activation as well as motility of T cells in various situations. Therefore, the outcome of tumor immunotherapy using checkpoint inhibitors is assumed to be closely related to the alteration of T cell motility, particularly in tumor-draining lymph nodes (TDLNs). In this review, we discuss the migration dynamics of T cells during their activation in TDLNs, and the roles of checkpoint molecules in T cell motility, to provide some insight into the effect of tumor immunotherapy via checkpoint blockade, in terms of T cell dynamics and the importance of TDLNs.

    DOI: 10.3390/cancers13184616

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  • Transdermal entry of yeast components elicits transient B cell-associated responses in skin-draining lymph nodes. 査読 国際誌

    Md Azizur Rahman, Yasuhiro Kanda, Madoka Ozawa, Toshihiko Kawamura, Arata Takeuchi, Tomoya Katakai

    Cellular immunology   355   104159 - 104159   2020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)  

    Immune responses to non-pathogenic yeasts induced within the draining lymph node remain to be understood. In this study, we have investigated the changes in lymphocytes and their activity in skin-draining lymph nodes in response to transdermally injected zymosan (component of the yeast cell wall). Zymosan elicited the transient increase of B cell number and activation status without affecting the capacity for proliferation. The increased B cell content in the regional lymph nodes was likely due to the reduction of B cell egress from the tissue and in part the increase of homing from the circulation. Zymosan also upregulated the inflammatory cytokines, such as IL-1β, IL-6, IL-12, and IFNγ, regulatory cytokines IL-10 and TGFβ, and lymphoid chemokine CXCL13. Among these, the expression of IL-12 and IL-10 was markedly high in B cells. Altogether, these findings demonstrate a unique B cell-associated response to non-pathogenic yeast component in the draining lymph nodes. This will provide insights into the clinical and healthcare applications of non-pathogenic beneficial microbes.

    DOI: 10.1016/j.cellimm.2020.104159

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  • PLOD2 Is Essential to Functional Activation of Integrin β1 for Invasion/Metastasis in Head and Neck Squamous Cell Carcinomas. 査読 国際誌

    Yushi Ueki, Ken Saito, Hidekazu Iioka, Izumi Sakamoto, Yasuhiro Kanda, Masakiyo Sakaguchi, Arata Horii, Eisaku Kondo

    iScience   23 ( 2 )   100850 - 100850   2020年2月

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    記述言語:英語  

    Identifying the specific functional regulator of integrin family molecules in cancer cells is critical because they are directly involved in tumor invasion and metastasis. Here we report high expression of PLOD2 in oropharyngeal squamous cell carcinomas (SCCs) and its critical role as a stabilizer of integrin β1, enabling integrin β1 to initiate tumor invasion/metastasis. Integrin β1 stabilized by PLOD2-mediated hydroxylation was recruited to the plasma membrane, its functional site, and accelerated tumor cell motility, leading to tumor metastasis in vivo, whereas loss of PLOD2 expression abrogated it. In accordance with molecular analysis, examination of oropharyngeal SCC tissues from patients corroborated PLOD2 expression associated with integrin β1 at the invasive front of tumor nests. PLOD2 is thus implicated as the key regulator of integrin β1 that prominently regulates tumor invasion and metastasis, and it provides important clues engendering novel therapeutics for these intractable cancers.

    DOI: 10.1016/j.isci.2020.100850

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  • Essential Role of Canonical NF-κB Activity in the Development of Stromal Cell Subsets in Secondary Lymphoid Organs. 査読 国際誌

    Bogdanova D, Takeuchi A, Ozawa M, Kanda Y, Rahman MA, Ludewig B, Kinashi T, Katakai T

    Journal of immunology (Baltimore, Md. : 1950)   201 ( 12 )   3580 - 3586   2018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)  

    DOI: 10.4049/jimmunol.1800539

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  • Visualizing the Rapid and Dynamic Elimination of Allogeneic T Cells in Secondary Lymphoid Organs. 査読 国際誌

    Kanda Y, Takeuchi A, Ozawa M, Kurosawa Y, Kawamura T, Bogdanova D, Iioka H, Kondo E, Kitazawa Y, Ueta H, Matsuno K, Kinashi T, Katakai T

    Journal of immunology (Baltimore, Md. : 1950)   201 ( 3 )   1062 - 1072   2018年8月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.4049/jimmunol.1700219

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  • A Distinct Subset of Fibroblastic Stromal Cells Constitutes the Cortex-Medulla Boundary Subcompartment of the Lymph Node. 査読 国際誌

    Takeuchi A, Ozawa M, Kanda Y, Kozai M, Ohigashi I, Kurosawa Y, Rahman MA, Kawamura T, Shichida Y, Umemoto E, Miyasaka M, Ludewig B, Takahama Y, Nagasawa T, Katakai T

    Frontiers in immunology   9   2196 - 2196   2018年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.3389/fimmu.2018.02196

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  • Extensively re-organized systemic lymph nodes provide a feasible environment for self-reactivity in lupus-prone NZB × NZW F1 mice. 査読

    Kurosawa Y, Ozawa M, Kanda Y, Takeuchi A, Kawamura T, Narita I, Katakai T

    International immunology   29 ( 12 )   567 - 579   2017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)  

    DOI: 10.1093/intimm/dxx066

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  • RASAL3, a novel hematopoietic RasGAP protein, regulates the number and functions of NKT cells 査読

    Suguru Saito, Toshihiko Kawamura, Masaya Higuchi, Takahiro Kobayashi, Manami Yoshita-Takahashi, Maya Yamazaki, Manabu Abe, Kenji Sakimura, Yasuhiro Kanda, Hiroki Kawamura, Shuying Jiang, Makoto Naito, Takumi Yoshizaki, Masahiko Takahashi, Masahiro Fujii

    EUROPEAN JOURNAL OF IMMUNOLOGY   45 ( 5 )   1512 - 1523   2015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)   出版者・発行元:WILEY-BLACKWELL  

    Ras GTPase-activating proteins negatively regulate the Ras/Erk signaling pathway, thereby playing crucial roles in the proliferation, function, and development of various types of cells. In this study, we identified a novel Ras GTPase-activating proteins protein, RASAL3, which is predominantly expressed in cells of hematopoietic lineages, including NKT, B, and Tcells. We established systemic RASAL3-deficient mice, and the mice exhibited a severe decrease in NKT cells in the liver at 8 weeks of age. The treatment of RASAL3-deficient mice with -GalCer, a specific agonist for NKT cells, induced liver damage, but the level was less severe than that in RASAL3-competent mice, and the attenuated liver damage was accompanied by a reduced production of interleukin-4 and interferon- from NKT cells. RASAL3-deficient NKT cells treated with -GalCer in vitro presented augmented Erk phosphorylation, suggesting that there is dysregulated Ras signaling in the NKT cells of RASAL3-deficient mice. Taken together, these results suggest that RASAL3 plays an important role in the expansion and functions of NKT cells in the liver by negatively regulating Ras/Erk signaling, and might be a therapeutic target for NKT-associated diseases.

    DOI: 10.1002/eji.201444977

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  • On/off switching of capillary vessel flow controls mitochondrial and glycolysis pathways for energy production 査読

    Toru Abo, Mayumi Watanabe, Chikako Tomiyama, Yasuhiro Kanda

    MEDICAL HYPOTHESES   83 ( 1 )   99 - 100   2014年7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:CHURCHILL LIVINGSTONE  

    Capillary vessel flow in the base of the fingernail can be observed by microscopy. This flow is switched off under some conditions, such as coldness, surprise, and anger and is switched on again under other conditions, such as warming, relaxation, and mild exercise. In other words, capillary vessels perform two functions: switching flow on and off. It is speculated that the switch-off function is necessary to direct energy production to the glycolysis pathway, while the switch-on function is necessary for the mitochondrial pathway. This is because glycolysis takes place under anaerobic conditions, while oxidative phosphorylation in the mitochondria proceeds under aerobic conditions in the body. To switch off circulation, the negative electric charges on the surface of erythrocytes and the capillary wall may be decreased by stimulation of the sympathetic nerves and secretion of steroid hormones. Negative charge usually acts as repulsive force between erythrocytes and between erythrocytes and the capillary wall. By decreasing the negative charge, erythrocytes can aggregate and also adhere to the capillary wall. These behaviors may be related to the capillary flow switch-off function. Here, it is emphasized that the capillary vessels possess not only a switch-on function but also a switch-off function for circulation. (C) 2014 Elsevier Ltd. All rights reserved.

    DOI: 10.1016/j.mehy.2014.03.035

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  • Reactivity of autoantibodies against not only erythrocytes but also hepatocytes in sera of mice with malaria 査読

    Yasuhiro Kanda, Toshihiko Kawamura, Takahiro Kobayashi, Hiroki Kawamura, Hisami Watanabe, Toru Abo

    CELLULAR IMMUNOLOGY   289 ( 1-2 )   162 - 166   2014年5月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    In order to further examine the reactivity of autoantibodies, mice were infected with a non-lethal strain of Plasmodium yoelii. Parasitemia appeared between days 10 and 21. During this period, hyperglycemia and hypothermia were serially obeserved and this phenomenon resembled stress-associated responses. In parallel with parasitemia, autoantibodies appeared against nucleus and double-stranded DNA in the sera. To examine further the reactivity of autoantibodies against tissues, immunohistochemical staining using sera from mice with or without malaria was conducted. Autoantibodies contained reactivity to erythrocytes in the spleen, bone marrow and peripheral blood, especially against tissues obtained from mice with malaria. In the liver and intestine, autoantibodies reacted with hepatocytes and intestinal epithelial cells, respectively. These results suggested that the reactivity of autoantibodies against erythrocytes and hepatocytes might be associated with the modulation of the disease course in malaria. (C) 2014 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.cellimm.2014.04.008

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  • Extracellular ATP-stimulated macrophages produce macrophage inflammatory protein-2 which is important for neutrophil migration 査読

    Hiroki Kawamura, Toshihiko Kawamura, Yasuhiro Kanda, Takahiro Kobayashi, Toru Abo

    IMMUNOLOGY   136 ( 4 )   448 - 458   2012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-BLACKWELL  

    Macrophages are the major source of the chemokines macrophage inflammatory protein-2 (MIP-2) and keratinocyte-derived chemokine (KC), which play a major role in neutrophil migration to sites of inflammation. Although extracellular ATP from inflammatory tissues induces several immune responses in macrophages, it is unclear whether ATP-stimulated macrophages affect neutrophil migration. Therefore, the aim of the present study was to investigate the role of ATP-induced MIP-2 production by macrophages. When ATP was injected intraperitoneally into mice, the number of neutrophils within the peritoneal cavity markedly increased, along with the levels of MIP-2 and KC in the peritoneal lavage fluid. Consistent with this, ATP induced MIP-2 production, but not that of KC, by peritoneal exudate macrophages (PEMs) in vitro. This occurred via interactions with the P2X7 receptor and P2Y2 receptor. Furthermore, treatment of PEMs with ATP led to the production of reactive oxygen species. The ATP-induced MIP-2 production was inhibited by treatment with the antioxidant N-acetyl-l-cysteine. Also, MIP-2 production was inhibited by pre-incubating PEMs with inhibitors of extracellular signal-regulated kinase 1/2 or p38 mitogen-activated protein kinase. The MIP-2 neutralization reduced the increase in neutrophil numbers observed in ATP-treated mice. Taken together, these results suggest that increased production of reactive oxygen species by ATP-stimulated macrophages activates the signalling pathways that promote MIP-2 production which, in turn, induces neutrophil migration.

    DOI: 10.1111/j.1365-2567.2012.03601.x

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  • Beta-Glucosylceramide Administration (i.p.) Activates Natural Killer T cells In Vivo and Prevents Tumor Metastasis in Mice 査読

    Masashi Inafuku, Changchun Li, Yasuhiro Kanda, Toshihiko Kawamura, Kazuyoshi Takeda, Hirosuke Oku, Hisami Watanabe

    LIPIDS   47 ( 6 )   581 - 591   2012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:SPRINGER HEIDELBERG  

    Natural killer (NK) T cells are well known to play important roles in both tumor rejection and the defense against infectious. Therefore, the antitumor potential of NKT cell-activating antigens have been the focus for the development of NKT cell-based immunotherapies. Up to now, several studies have revealed that the administrations of glycolipids (e.g. alpha-galactosylceramide) can successfully treat certain metastatic tumors. However, liver injuries appeared upon the application of these antigens. We previously examined the potential of using beta-glucosylceramide (beta-GlcCer) to inhibit tumor metastasis to the liver. The aim of this study was to determine the antimetastatic effects of beta-GlcCer and its impact on the activation of NKT cells. Intraperitoneal administration of beta-GlcCer enhanced the production of interferon-gamma from hepatic lymphocytes containing NKT cells, and increased the cytotoxicity of hepatic lymphocytes against tumor cells. Moreover, beta-GlcCer administration suppressed the hepatic metastasis of tumors in wild type (WT) mice, but not in CD1d (-/-) or J alpha 18 (-/-) mice. The drawback associated with the other glycolipids in liver injury was not noted in WT mice treated with the continuous daily administration of beta-GlcCer for 2 weeks. The present study demonstrated that beta-GlcCer treatment activates invariant NKT cells, thus resulting in the inhibition of tumor metastasis.

    DOI: 10.1007/s11745-012-3666-1

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  • Natural killer T cells suppress zymosan A-mediated granuloma formation in the liver by modulating interferon-γ and interleukin-10. 査読

    Kobayashi T, Kawamura H, Kanda Y, Matsumoto H, Saito S, Takeda K, Kawamura T, Abo T

    Immunology   136 ( 1 )   86 - 95   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: 10.1111/j.1365-2567.2012.03562.x

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  • Coincidence of autoantibody production with the activation of natural killer T cells in α-galactosylceramide-mediated hepatic injury. 査読

    Matsumoto H, Kawamura T, Kobayashi T, Kanda Y, Kawamura H, Abo T

    Immunology   133 ( 1 )   21 - 28   2011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: 10.1111/j.1365-2567.2011.03405.x

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  • Identification and characterization of autoantibody-producing B220(low) B (B-1) cells appearing in malarial infection 査読

    Yasuhiro Kanda, Hiroki Kawamura, Hiroaki Matsumoto, Takahiro Kobayashi, Toshihiko Kawamura, Toru Abo

    CELLULAR IMMUNOLOGY   263 ( 1 )   49 - 54   2010年

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    Mice with malaria showed unique immunological responses, including the expansion of NK1.1(-)TCR(int) cells (extrathymic T cells). Since TCR(int) cells with autoreactivity and autoantibody-producing B cells (B-1 cells) are often simultaneously activated under autoimmune conditions, it was examined whether B-1 cells were activated in the course of malarial infection. From days 14 after infection, B220(low) B-1 cells appeared in the liver and spleen. The number of B220(low) B cells was highest at day 14, but the ratio was highest at days 28-35. In parallel with the appearance of B220(low) cells, autoantibodies against HEp-2 cells and double-stranded DNA were detected in sera. These B220(low) cells had phenotypes of CD44(high), CD23(-) and CD62L(-). In sharp contrast, conventional B220(high) B cells (B-2 cells) were CD44(low), CD23(+) and CD62L(+). These results suggested that malaria immune responses were not mediated by conventional T and B cells but resembled the responses during autoimmune diseases. (C) 2010 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.cellimm.2010.02.015

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  • Co-appearance of autoantibody-producing B220(low) B cells with NKT cells in the course of hepatic injury 査読

    Yuki Fujii, Hiroki Kawamura, Toshihiko Kawamura, Yasuhiro Kanda, Hiroaki Matsumoto, Takahiro Kobayashi, Takashi Yamamoto, Takashi Aoyama, Toru Abo

    CELLULAR IMMUNOLOGY   260 ( 2 )   105 - 112   2010年

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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:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    Severe hepatic injury is induced by Concanavalin A (Con A) administration in mice, the major effector cells being CD4(+) T cells, NKT cells and macrophages. Since autologous lymphocyte subsets are associated with tissue damage, Con A-induced hepatic injury is considered to be autoimmune hepatitis. However, it has remained to be investigated how autoantibodies and B-1 cells are responsible for this phenomenon. In this study, it was demonstrated that autoantibodies which were detected using Hep-2 cells in immunofluorescence tests and using double-strand (ds) DNA in the ELISA method, appeared after Con A administration (a peak at day 14). Moreover, autoantibody-producing B220(low) cells (i.e., B-1 cells) also appeared at this time. Purified B220(low) cells were found to have a potential to produce autoantibodies. These results suggest that Con A-induced hepatic injury indeed includes the mechanism of autoimmune hepatitis. (C) 2009 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.cellimm.2009.09.009

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  • Appearance of B220low autoantibody-producing B-1 cells at neonatal and older stages in mice. 査読

    Tachikawa S, Kawamura T, Kawamura H, Kanda Y, Fujii Y, Matsumoto H, Abo T

    Clinical and experimental immunology   153 ( 3 )   448 - 455   2008年9月

  • Malaria protection in beta(2)-microglobulin-deficient mice lacking major histocompatibility complex class I antigens: essential role of innate immunity, including gamma delta T cells 査読

    Tomoyo Taniguchi, Saoko Tachikawa, Yasuhiro Kanda, Toshihiko Kawamura, Chikako Tomiyama-Miyaji, Changchun Li, Hisami Watanabe, Hiroho Sekikawa, Toru Abo

    IMMUNOLOGY   122 ( 4 )   514 - 521   2007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:BLACKWELL PUBLISHING  

    It is still controversial whether malaria protection is mediated by conventional immunity associated with T and B cells or by innate immunity associated with extrathymic T cells and autoantibody-producing B cells. Given this situation, it is important to examine the mechanism of malaria protection in beta(2)-microglobulin-deficient (beta(2)m(-/-)) mice. These mice lack major histocompatibility complex class I and CD1d antigens, which results in the absence of CD8(+) T cells and natural killer T (NKT) cells. When C57BL/6 and beta(2)m(-/-) mice were injected with parasitized (Plasmodium yoelii 17XNL) erythrocytes, both survived from the infection and showed a similar level of parasitaemia. The major expanding T cells were NK1.1(-) alpha beta T-cell receptor(int) cells in both mice. The difference was a compensatory expansion of NK and gamma delta T cells in beta(2)m(-/-) mice, and an elimination experiment showed that these lymphocytes were critical for protection in these mice. These results suggest that malaria protection might be events of the innate immunity associated with multiple subsets with autoreactivity. CD8(+) T and NKT cells may be partially related to this protection.

    DOI: 10.1111/j.1365-2567.2007.02661.x

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  • Modulation of the endocrine and immune systems by well-controlled hyperthermia equipment 査読

    Chikako Tomiyama-Miyaji, Mayumi Watanabe, Takahiko Ohishi, Yasuhiro Kanda, Eisuke Kainuma, Hanaa Y. Bakir, JiWei Shen, HongWei Ren, Masashi Inoue, Keiho Tajima, XueFeng Bai, Toru Abo

    BIOMEDICAL RESEARCH-TOKYO   28 ( 3 )   119 - 125   2007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:BIOMEDICAL RESEARCH PRESS LTD  

    Since high levels of hyperthermia induce immunosuppression to a certain extent (i.e., granulocytosis and lymphocytopenia) in patients, we applied mild hyperthermia in volunteers using equipment enabling well-controlled hyperthermia. Restricted control of rectal temperature at 39.4 (+/- 0.2)degrees C for 30 min was conducted and various parameters of the body were examined. The most prominent change observed during exposure to hyperthermia was elevated levels of pH and PO2 in the blood, even in the venous blood. A transient elevation of ACTH, cortisol and growth hormone in the blood was also seen during this time. In parallel with this phenomenon, the number of total lymphocytes and those of its subsets (especially CD57(+) or CD56(+) NK cells and NKT cells) increased. More interestingly, the proportion of HLA-DR (MHC class II antigens) increased in NK and NKT cells, and their intensity on the Surface of CD20(+) B cells increased. These results suggest that mild hyperthermia is important for modulation of the functions of the circulatory, endocrine and immune systems.

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  • Relationship between diseases accompanied by tissue destruction and granulocytes with surface adrenergic receptors 査読

    Toru Abo, Toshihiko Kawamura, Hiroki Kawamura, Chikako Tomiyama-Miyaji, Yasuhiro Kanda

    IMMUNOLOGIC RESEARCH   37 ( 3 )   201 - 210   2007年

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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:HUMANA PRESS INC  

    It is well-known that physiological phenomena and certain diseases, including neonatal granulocytosis, age-associated granulocytosis, periodontitis, pancreatitis, Crohn's disease, ulcerative colitis, hemorrhoids, endometriosis, and NSADs-enteritis, are accompanied by tissue destruction and granulocytosis. We investigated what is a key factor connecting tissue destruction and granulocytosis, attention being, focused on adrenergic receptors on granulocytes and stress-induced sympathetic nerve stimulation. If we introduce the concept that "granulocytosis and subsequent tissue destruction are induced by sympathetic nerve stimulation," the mechanisms underlying many physiological phenomena and the etiology of several uncurable diseases in humans can be clearly understood.

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  • Activation of CD1d-independent NK1.1(+) T cells in the large intestine by Lactobacilli 査読

    S Takahashi, T Kawamura, Y Kanda, T Taniguchi, T Nishizawa, T Iiai, K Hatakeyama, T Abo

    IMMUNOLOGY LETTERS   102 ( 1 )   74 - 78   2006年1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:ELSEVIER SCIENCE BV  

    Among digestive organs, the liver and the large intestine are abundant in T cells expressing NK1.1. NK1.1(+) T cells in the liver are mostly CD1d-dependent whereas those in the large intestine are CD1d-independent. In this study, we investigated the effects of Lactobacilli on NK1.1(+) T cells in the digestive organs of mice. C57BL/6 mice were orally given a dietary supplement prepared from mixed cultures of eight strains of Lactobacilli. Oral administration of Lactobacilli to mice resulted in the selective expansion of NK1.1(+) T cells in the large intestine. These colon NK1.1(+) T cells activated by Lactobacilli were found to express IFN-gamma mRNA. The level of IFN-gamma in the serum was also elevated by the administration of Lactobacilli. Our results suggest that Lactobacilli selectively activate CD1d-independent NK1.1(+) T cells in the large intestine to produce IFN-gamma and therefore modulate Th1 immune responses. (c) 2005 Published by Elsevier B.V.

    DOI: 10.1016/j.imlet.2005.07.003

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  • Multipotential acceptance of Peyer's patches in the intestine for both thymus-derived T cells and extrathymic T cells in mice 査読

    S Takahashi, T Kawamura, Y Kanda, T Taniguchi, T Nishizawa, T Iiai, K Hatakeyama, T Abo

    IMMUNOLOGY AND CELL BIOLOGY   83 ( 5 )   504 - 510   2005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:BLACKWELL PUBLISHING  

    Peyer's patches (PP) are important inductive sites for the mucosal immune response. It is well known that lymphocytes that migrate into PP are mainly of T-cell lineage from thymus-derived cells (i.e. alpha beta TCRhigh cells). In this study, we further characterized the properties of PP lymphocytes in mice using a mouse model of colitis induced by dextran sulphate sodium (DSS). Although the major site of the inflammation induced by DSS is known to be the large intestine, the small intestine was also damaged. When mice developed DSS-induced colitis, CD3(+)CD8(+)B220(+)gamma delta T cells increased in PP in the small intestine. These gamma delta T cells, which are not seen in the PP of normal mice, resembled intraepithelial lymphocytes (IEL) in the small intestine in terms of their expression of CD5, CD103 and Thy1.2. In addition, the V gamma/delta repertoire of these gamma delta T cells was similar to that of gamma delta IEL. When DSS-treated mice were injected with IEL isolated from normal mice, IEL including gamma delta T cells preferentially migrated to PP, raising the possibility that B220(+) T cells seen in PP of diseased mice may derive from IEL in the small intestine. Our present study suggests that PP might be able to accept T-cell lineages from intestinal IEL as well as from thymus-derived T cells.

    DOI: 10.1111/j.1440-1711.2005.01361.x

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    PubMed

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書籍等出版物

  • Handbook of Granulocytes: Classification, Toxic Materials Produced and Pathology

    ( 担当: 共著 ,  範囲: Role of granulocytes on the onset of tissue-destructive diseases when exposed to stress)

    Nova Science Publishers Inc.  2009年 

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担当経験のある授業科目(researchmap)

  • 生体防御と感染(免疫学)

    機関名:新潟大学

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  • 感染防御と感染(医動物学)

    機関名:新潟大学

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