西川 陽太郎 (ニシカワ ヨウタロウ)

NISHIKAWA Yotaro

写真a

所属

医学部 附属病院 皮膚科

職名

講師

外部リンク

学位 【 表示 / 非表示

  • 博士(医学) ( 2022年3月   宮崎大学 )

 

論文 【 表示 / 非表示

  • Congenital Deficiency of Conventional Dendritic Cells Promotes the Development of Atopic Dermatitis-Like Inflammation 査読あり 国際共著

    Nishikawa Y., Fukaya T., Fukui T., Uto T., Takagi H., Nasu J., Miyanaga N., Riethmacher D., Choijookhuu N., Hishikawa Y., Amano M., Sato K.

    Frontiers in Immunology   12   712676   2021年7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:Frontiers in Immunology  

    Atopic dermatitis (AD) is a common pruritic inflammatory skin disease characterized by impaired epidermal barrier function and dysregulation of Thelper-2 (TH2)-biased immune responses. While the lineage of conventional dendritic cells (cDCs) are implicated to play decisive roles in T-cell immune responses, their requirement for the development of AD remains elusive. Here, we describe the impact of the constitutive loss of cDCs on the progression of AD-like inflammation by using binary transgenic (Tg) mice that constitutively lacked CD11chi cDCs. Unexpectedly, the congenital deficiency of cDCs not only exacerbates the pathogenesis of AD-like inflammation but also elicits immune abnormalities with the increased composition and function of granulocytes and group 2 innate lymphoid cells (ILC2) as well as B cells possibly mediated through the breakdown of the Fms-related tyrosine kinase 3 ligand (Flt3L)-mediated homeostatic feedback loop. Furthermore, the constitutive loss of cDCs accelerates skin colonization of Staphylococcus aureus (S. aureus), that associated with disease flare. Thus, cDCs maintains immune homeostasis to prevent the occurrence of immune abnormalities to maintain the functional skin barrier for mitigating AD flare.

    DOI: 10.3389/fimmu.2021.712676

    Scopus

    PubMed

  • Clec4A4 Acts As A Negative Immune Checkpoint Regulator to Suppress Antitumor Immunity. 査読あり

    Uto T, Fukaya T, Mitoma S, Nishikawa Y, Tominaga M, Choijookhuu N, Hishikawa Y, Sato K

    Cancer immunology research   2023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)  

    DOI: 10.1158/2326-6066.CIR-22-0536

    PubMed

  • Gut dysbiosis promotes the breakdown of oral tolerance mediated through dysfunction of mucosal dendritic cells 査読あり

    Fukaya T., Uto T., Mitoma S., Takagi H., Nishikawa Y., Tominaga M., Choijookhuu N., Hishikawa Y., Sato K.

    Cell Reports   42 ( 5 )   112431   2023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:Cell Reports  

    While dysbiosis in the gut is implicated in the impaired induction of oral tolerance generated in mesenteric lymph nodes (MesLNs), how dysbiosis affects this process remains unclear. Here, we describe that antibiotic-driven gut dysbiosis causes the dysfunction of CD11c+CD103+ conventional dendritic cells (cDCs) in MesLNs, preventing the establishment of oral tolerance. Deficiency of CD11c+CD103+ cDCs abrogates the generation of regulatory T cells in MesLNs to establish oral tolerance. Antibiotic treatment triggers the intestinal dysbiosis linked to the impaired generation of colony-stimulating factor 2 (Csf2)-producing group 3 innate lymphoid cells (ILC3s) for regulating the tolerogenesis of CD11c+CD103+ cDCs and the reduced expression of tumor necrosis factor (TNF)-like ligand 1A (TL1A) on CD11c+CD103+ cDCs for generating Csf2-producing ILC3s. Thus, antibiotic-driven intestinal dysbiosis leads to the breakdown of crosstalk between CD11c+CD103+ cDCs and ILC3s for maintaining the tolerogenesis of CD11c+CD103+ cDCs in MesLNs, responsible for the failed establishment of oral tolerance.

    DOI: 10.1016/j.celrep.2023.112431

    Scopus

    PubMed

  • 症例報告 アダリムマブと植皮術が有効であった壊疽性膿皮症の1例 査読あり

    森 愛菜, 西川 陽太郎, 中村 俊央, 天野 正宏

    臨床皮膚科   77 ( 6 )   457 - 462   2023年5月

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    記述言語:日本語   掲載種別:症例報告   出版者・発行元:株式会社医学書院  

    DOI: 10.11477/mf.1412207020

    CiNii Research

  • 症例報告 ボリコナゾール長期内服による多発有棘細胞癌の治療中に生じたMerkel細胞癌の1例 査読あり

    森 愛菜, 持田 耕介, 西川 陽太郎, 中村 俊央, 魏 峻洸, 河野 徳明, 天野 正宏

    臨床皮膚科   77 ( 6 )   433 - 438   2023年5月

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    記述言語:日本語   掲載種別:研究論文(学術雑誌)   出版者・発行元:株式会社医学書院  

    DOI: 10.11477/mf.1412207016

    CiNii Research

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