Faculty of Medicine College Hospital Dermatology



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Degree 【 display / non-display

  • 博士(医学) ( 2022.3   宮崎大学 )


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  • Congenital Deficiency of Conventional Dendritic Cells Promotes the Development of Atopic Dermatitis-Like Inflammation Reviewed International coauthorship

    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   2021.7

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



  • Clec4A4 Acts As A Negative Immune Checkpoint Regulator to Suppress Antitumor Immunity. Reviewed

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

    Cancer immunology research   2023.7

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

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


  • Gut dysbiosis promotes the breakdown of oral tolerance mediated through dysfunction of mucosal dendritic cells Reviewed

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

    Cell Reports   42 ( 5 )   112431   2023.5

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



  • 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 Reviewed

    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   2023.5

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    Language:Japanese   Publishing type:Case report   Publisher:株式会社医学書院  

    DOI: 10.11477/mf.1412207020

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  • 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 Reviewed

    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   2023.5

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    Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:株式会社医学書院  

    DOI: 10.11477/mf.1412207016

    CiNii Research

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