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Faculty of Medicine College Hospital Dermatology |
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NISHIKAWA Yotaro
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Papers 【 display / non-display 】
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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
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.
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当科におけるHTLV－1キャリアの皮膚症状の検討 Reviewed
野上 京子, 成田 幸代, 西川 陽太郎, 持田 耕介, 前久保 理恵, 瀬戸山 充, 天野 正宏
Ｓｋｉｎ Ｃａｎｃｅｒ 39 ( 3 ) 230 - 236 2025.2
Language：Japanese Publishing type：Research paper (scientific journal) Publisher：日本皮膚悪性腫瘍学会
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症例 ペムブロリズマブによる免疫関連有害事象と考えられたHypertrophic Lichen Planusの1例 Reviewed
後田 優香, 西川 陽太郎, 野海 健太, 魏 峻洸, 天野 正宏
皮膚科の臨床 65 ( 12 ) 1896 - 1899 2023.11
Language：Japanese Publishing type：Case report Publisher：金原出版
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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 11 ( 9 ) 1266 - 1279 2023.7
Language：English Publishing type：Research paper (scientific journal) Publisher：Cancer Immunology Research
Clec4A4 is a C-Type lectin receptor (CLR) exclusively expressed on murine conventional dendritic cells (cDC) to regulate their activation status. However, the functional role of murine Clec4A4 (mClec4A4) in antitumor immunity remains unclear. Here, we show that mClec4A4 serves as a negative immune checkpoint regulator to impair antitumor immune responses. Deficiency of mClec4A4 lead to a reduction in tumor development, accompanied by enhanced antitumor immune responses and amelioration of the immunosuppressive tumor microenvironment (TME) mediated through the enforced activation of cDCs in tumor-bearing mice. Furthermore, antagonistic mAb to human CLEC4A (hCLEC4A), which is the functional orthologue of mClec4A4, exerted protection against established tumors without any apparent signs of immunerelated adverse events in hCLEC4A-Transgenic mice. Thus, our findings highlight the critical role of mClec4A4 expressed on cDCs as a negative immune checkpoint molecule in the control of tumor progression and provide support for hCLEC4A as a potential target for immune checkpoint blockade in tumor immunotherapy.
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Choijookhuu Narantsog, Hishikawa Yoshitaka, Sato Katsuaki, Fukaya Tomohiro, Uto Tomofumi, Mitoma Shuya, Takagi Hideaki, Nishikawa Yotaro, Tominaga Moe
Cell Reports 42 ( 5 ) 112431 2023.5
Language：English Publishing type：Research paper (scientific journal)
Grant-in-Aid for Scientific Research 【 display / non-display 】
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IL-22結合タンパクによるアトピー性皮膚炎の制御機構の解明と治療法の開発
Grant number：24K19177 2024.04 - 2028.03
独立行政法人日本学術振興会 科学研究費基金 若手研究
Authorship：Principal investigator