Details of a Researcher - EBIHARA Takashi

EBIHARA Takashi

写真a

Affiliation	Graduate School of Medicine Doctorial Course in Medicine Bioregulatory Medicine Department of Medical Biology
Date of Birth	1972
Laboratory Address	1-1-1 Hondo, Akita 010-8543, Japan
Laboratory Phone number	+81-18-884-6080
Mail Address

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Research Interests 【 display / non-display 】

Chronic inflammation
Allergy
Infectious diseases
Immunity
Transcriptional regulation

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Graduating School 【 display / non-display 】

　

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1998.03

Hokkaido University Faculty of Medicine Graduated
1992.04

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1998.03

Hokkaido University Faculty of Medicine Graduated

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Campus Career 【 display / non-display 】

2019.04

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Now

Akita University Graduate School of Medicine Doctorial Course in Medicine Bioregulatory Medicine Professor

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Academic Society Affiliations 【 display / non-display 】

2013.09

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Now

Japan

Japanese Society for Immunology

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Research Areas 【 display / non-display 】

Life Science / Experimental pathology
Life Science / Immunology / 自然リンパ球、NK細胞
Life Science / Experimental pathology / アレルギー、ウイルス感染、細菌感染

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Research Career 【 display / non-display 】

Pediatric diseases caused by new emergent viruses including human metapneumovirus

Grant-in-Aid for Scientific Research

Periods of research：

2002.04

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2005.03

Classification of research form：Individual

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Research Achievements 【 display / non-display 】

◆Original paper【 display / non-display 】

TIGIT mediates activation-induced cell death of ILC2s during chronic airway allergy.

Toshiki Yamada, Megumi Tatematsu, Shunsuke Takasuga, Akane Fuchimukai, Kenki Yamagata, Shinsuke Seki, Keiji Kuba, Hideyuki Yoshida, Ichiro Taniuchi, Günter Bernhardt, Kazuko Shibuya, Akira Shibuya, Takechiyo Yamada, Takashi Ebihara

The Journal of experimental medicine ( The Journal of experimental medicine ) 220 ( 7 ) 2023.07 [Refereed]

Research paper (journal) International Co-author

While group-2 innate lymphoid cells (ILC2s) are highly proliferative in allergic inflammation, the removal of overactivated ILC2s in allergic diseases has not been investigated. We previously showed that chronic airway allergy induces "exhausted-like" dysfunctional ILC2s expressing T cell immunoreceptor with Ig and ITIM domains (TIGIT). However, the physiological relevance of these cells in chronic allergy remains elusive. To precisely identify and monitor TIGIT+ ILC2s, we generated TIGIT lineage tracer mice. Chronic allergy stably induced TIGIT+ ILC2s, which were highly activated, apoptotic, and were quickly removed from sites of chronic allergy. Transcripts from coding genes were globally suppressed in the cells, possibly due to reduced chromatin accessibility. Cell death in TIGIT+ ILC2s was enhanced by interactions with CD155 expressed on macrophages, whereas genetic ablation of Tigit or blockade by anti-TIGIT antagonistic antibodies promoted ILC2 survival, thereby deteriorating chronic allergic inflammation. Our work demonstrates that TIGIT shifts the fate of ILC2s toward activation-induced cell death, which could present a new therapeutic target for chronic allergies.

DOI PubMed

Quantification of Aspergillus fumigatus antigen Asp f 1 in airway tissue and allergic inflammation

Yui Miyabe, Hiroki Tomizawa, Hidekazu Saito, Toshiki Yamada, Kazuhiro Shiina, Koh Koizumi, Yohei Kawasaki, Shinsuke Suzuki, Mineyo Fukuchi, Shigeharu Ueki, Takashi Ebihara, Takechiyo Yamada

Allergy ( Wiley ) 77 ( 10 ) 3154 - 3156 2022.10 [Refereed]

Research paper (journal)

DOI

Identification of Galectin-7 as a crucial metastatic enhancer of squamous cell carcinoma associated with immunosuppression

An J.

Oncogene ( Oncogene ) 2022 [Refereed]

Research paper (journal)

DOI

Trained innate lymphoid cells in allergic diseases

Ebihara Takashi, Tatematsu Megumi, Fuchimukai Akane, Yamada Toshiki, Yamagata Kenki, Takasuga Shunsuke, Yamada Takechiyo

Allergology International ( 一般社団法人日本アレルギー学会 ) 70 ( 2 ) 174 - 180 2021 [Refereed] [Invited]

Research paper (journal)

Group 2 innate lymphoid cells (ILC2s) reside in peripheral tissues such as the lungs, skin, nasal cavity, and gut and provoke innate type 2 immunity against allergen exposure, parasitic worm infection, and respiratory virus infection by producing TH2 cytokines. Recent advances in understanding ILC2 biology revealed that ILC2s can be trained by IL-33 or allergic inflammation, are long-lived, and mount memory-like type 2 immune responses to any other allergens afterwards. In contrast, IL-33, together with retinoic acid, induces IL-10-producing immunosuppressive ILC2s. In this review, we discuss how the allergic cytokine milieu and other immune cells direct the generation of trained ILC2s with immunostimulatory or immunosuppressive recall capability in allergic diseases and infections associated with type 2 immunity. The molecular mechanisms of trained immunity by ILCs and the physiological relevance of trained ILC2s are also discussed.

DOI

Exhausted-like Group 2 Innate Lymphoid Cells in Chronic Allergic Inflammation

Ebihara T, Taniuchi I

Trends in Immunology ( Trends in Immunology ) 40 ( 12 ) 1095 - 1104 2019.12 [Refereed] [Invited]

Research paper (journal) Domestic Co-author

DOI

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◆Introduction and explanation【 display / non-display 】

Trained immunity and innate lymphoid cell memory

80 ( 1 ) 22 - 28 2023.07

Introduction and explanation (scientific journal)

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◆Other【 display / non-display 】

Ccr4-NOT脱アデニル化酵素複合体は抗腫瘍性NK細胞活性を制御する(The Ccr4-Not deadenylase complex controls antitumor NK cell activity)

Tatematsu Megumi, Sawa Shinichiro, Ikuta Koichi, Ebihara Takashi

日本免疫学会総会・学術集会記録 ( (NPO)日本免疫学会 ) 50 ( Proceedings ) 3 - P 2021.11