Amagai, Masayuki

写真a

Affiliation

School of Medicine, Department of Dermatology (Shinanomachi)

Position

Professor

External Links

Other Affiliation 【 Display / hide

  • Dean, School of Medicine

Academic Degrees 【 Display / hide

  • 医学博士, Keio University, 1989.11

 

Research Areas 【 Display / hide

  • Dermatology

Research Keywords 【 Display / hide

  • 皮膚免疫学

  • 皮膚診断学

 

Books 【 Display / hide

  • 慶應義塾大学病院の医師100人と学病気の予習帳

    AMAGAI MASAYUKI, 講談社:東京, 2017.02

    Scope: 186

  • 臨床検査データブック2017-2018

    AMAGAI MASAYUKI, 医学書院:東京, 2017.02

    Scope: 452-453

  • 臨床検査データブック2017-2018

    AMAGAI MASAYUKI, 医学書院:東京, 2017.02

    Scope: 451-452

  • 臨床検査データブック2017-2018

    AMAGAI MASAYUKI, 医学書院:東京, 2017.02

    Scope: 452

  • 皮膚科研修ノート

    AMAGAI MASAYUKI, 診断と治療社, 2016.04

    Scope: 51-53

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Papers 【 Display / hide

  • Co-activation of macrophages and T cells contribute to chronic GVHD in human IL-6 transgenic humanised mouse model

    Ono R., Watanabe T., Kawakami E., Iwasaki M., Tomizawa-Murasawa M., Matsuda M., Najima Y., Takagi S., Fujiki S., Sato R., Mochizuki Y., Yoshida H., Sato K., Yabe H., Kato S., Saito Y., Taniguchi S., Shultz L., Ohara O., Amagai M., Koseki H., Ishikawa F.

    EBioMedicine (EBioMedicine)  41   584 - 596 2019.03

     View Summary

    © 2019 The Authors Background: Graft-versus host disease (GVHD) is a complication of stem cell transplantation associated with significant morbidity and mortality. Non-specific immune-suppression, the mainstay of treatment, may result in immune-surveillance dysfunction and disease recurrence. Methods: We created humanised mice model for chronic GVHD (cGVHD) by injecting cord blood (CB)-derived human CD34 + CD38 − CD45RA − haematopoietic stem/progenitor cells (HSPCs) into hIL-6 transgenic NOD/SCID/Il2rgKO (NSG) newborns, and compared GVHD progression with NSG newborns receiving CB CD34 − cells mimicking acute GVHD. We characterised human immune cell subsets, target organ infiltration, T-cell repertoire (TCR) and transcriptome in the humanised mice. Findings: In cGVHD humanised mice, we found activation of T cells in the spleen, lung, liver, and skin, activation of macrophages in lung and liver, and loss of appendages in skin, obstruction of bronchioles in lung and portal fibrosis in liver recapitulating cGVHD. Acute GVHD humanised mice showed activation of T cells with skewed TCR repertoire without significant macrophage activation. Interpretation: Using humanised mouse models, we demonstrated distinct immune mechanisms contributing acute and chronic GVHD. In cGVHD model, co-activation of human HSPC-derived macrophages and T cells educated in the recipient thymus contributed to delayed onset, multi-organ disease. In acute GVHD model, mature human T cells contained in the graft resulted in rapid disease progression. These humanised mouse models may facilitate future development of new molecular medicine targeting GVHD.

  • Rituximab therapy for refractory autoimmune bullous diseases: A multicenter, open-label, single-arm, phase 1/2 study on 10 Japanese patients

    Kurihara Y., Yamagami J., Funakoshi T., Ishii M., Miyamoto J., Fujio Y., Kakuta R., Tanikawa A., Aoyama Y., Iwatsuki K., Ishii N., Hashimoto T., Nishie W., Shimizu H., Kouyama K., Amagai M.

    Journal of Dermatology (Journal of Dermatology)  46 ( 2 ) 124 - 130 2019.02

    ISSN  03852407

     View Summary

    © 2018 Japanese Dermatological Association This was a multicenter study of rituximab, a chimeric monoclonal immunoglobulin G antibody directed against CD20, for the treatment of refractory autoimmune bullous diseases (pemphigus and pemphigoid). Ten patients (three with pemphigus vulgaris, six with pemphigus foliaceus and one with bullous pemphigoid) were treated with a single cycle of rituximab (four weekly infusions at a dose of 375 mg/m 2 of body surface area). The primary end-points were the number of serious adverse events and rate of complete remission at 40 weeks. Five patients (50%) achieved complete remission with minimal therapy (defined as no active lesions with lower doses of systemic corticosteroids compared to that with prednisolone 10 mg/day). Improvements in clinical scores (Pemphigus Disease Area Index) and decreases in autoantibody titers in the sera were observed in the four pemphigus patients who failed to achieve complete remission. This suggests that rituximab was effective in nine of 10 cases. Two serious adverse events (Pneumocystis carinii pneumonia and septic shock due to infectious arthritis) were observed and adequately treated with hospitalization. CD19-positive B lymphocytes in the peripheral blood decreased on day 29 following rituximab treatment, and remained at low levels throughout the observation period (280 days). Our results confirmed the efficacy of rituximab therapy for refractory autoimmune bullous diseases in Japan.

  • Identification of a human papillomavirus type 58 lineage in multiple Bowen's disease on the fingers: Case report and published work review

    Kobayashi K., Tanese K., Kubo A., Matsumoto-Mochimaru N., Sasaki A., Kameyama K., Amagai M., Umegaki-Arao N.

    Journal of Dermatology (Journal of Dermatology)  45 ( 10 ) 1195 - 1198 2018.10

    ISSN  03852407

     View Summary

    © 2018 Japanese Dermatological Association Human papillomavirus (HPV) has been detected in some cases of Bowen's disease, particularly on the fingers and genitalia. HPV-58 is classified as a high-risk mucosal type and accounts for a high percentage of cervical cancer in Asia. Moreover, several HPV-58 lineages, including sublineage A1, have a high prevalence in Asia. However, the nature of HPV-58-associated skin cancer is still unknown. Here, we report a case of a Japanese patient with multiple Bowen's disease on the fingers. A 33-year-old man presented with multiple reddish-brown scaly plaques on his left middle finger and right ring finger. All lesions were surgically excised, and the diagnosis of Bowen's disease was made. We performed Sanger sequencing using DNA extracted from paraffin-embedded samples and identified HPV-58 sublineage A1. Additionally, we review previous reports on HPV-58-associated skin cancers, including our case, showing a high regional prevalence in Asia. Further studies would be needed to reveal the relationship between HPV-58 lineages and carcinogenesis in the skin.

  • Vancomycin mediates IgA autoreactivity in drug-induced linear IgA bullous dermatosis

    Yamagami, J. Nakamura, Y. Nagao, K. Funakoshi, T. Takahashi, H. Tanikawa, A. Hachiya, T. Yamamoto, T. Ishida-Yamamoto, A. Tanaka, T. Fujimoto, N. Nishigori, C. Yoshida, T. Ishii, N. Hashimoto, T. Amagai, M.

    J Invest Dermatol (Journal of Investigative Dermatology)  138 ( 7 ) 1473 - 1480 2018.07

    Accepted,  ISSN  0022202X

     View Summary

    © 2018 The Authors Vancomycin (VCM) is known to induce linear IgA bullous dermatosis (LAD). However, in contrast to conventional LAD, in which circulating IgA autoantibodies against basement membrane proteins are commonly detected, patient sera from VCM-induced LAD yields negative results in indirect immunofluorescence microscopy, and the targeted autoantigen remains undetermined. By using sera from a typical patient with VCM-induced LAD, we identified that co-incubation of sera with VCM resulted in linear IgA deposition at the basement membrane zone by indirect immunofluorescence. Patient sera reacted with the dermal side of 1 mol/L NaCl-split skin and with the recombinant noncollagenous (i.e., NC1) domain of type VII collagen by both immunoblot and ELISA in the presence of VCM. The investigation of an additional 13 patients with VCM-induced LAD showed that 10 out of the 14 sera (71.4%) reacted with the NC1 domain of type VII collagen by ELISA when spiked with VCM, whereas only 4 (28.6%) tested positive without it. The enhancement of reactivity to NC1 by VCM, as determined by optical density via ELISA, was observed in 10 out of the 14 sera (71.4%). These findings indicate that type VII collagen is a target autoantigen in VCM-induced LAD and that VCM mediates IgA autoreactivity against type VII collagen, providing an insight into mechanisms involved in drug-induced autoimmune disease.

  • Characterization of centriole duplication in human epidermis, Bowen's disease, and squamous cell carcinoma

    Watanuki, S. Fujita, H. Kouyama, K. Amagai, M. Kubo, A.

    J Dermatol Sci (Journal of Dermatological Science)  91 ( 1 ) 9 - 18 2018.07

    Joint Work, Accepted,  ISSN  09231811

     View Summary

    © 2018 Background: Centrosomes contain two centrioles: a pre-existing mature centriole and a newly formed immature centriole. Each centriole is duplicated once within a cell cycle, which is crucial for proper centrosome duplication and cell division. Objective: To describe the centrosome duplication cycle in human epidermis, Bowen's disease (BD), and squamous cell carcinoma (SCC). Methods: Immunofluorescent staining of centriolar proteins and Ki-67 was used to evaluate cell cycles and the number of centrioles. Centrobin and Outer dense fiber of sperm tails 2 (ODF2) were used as markers for immature and mature centrioles, respectively. Results: Normal human primary epidermal keratinocytes in a monolayered culture have one centrobin+ centriole (CTRB1+ cells) supposed in G0/G1 phases or have two centrobin+ centrioles (CTRB2+ cells) supposed in S−G2 phase. In a three-dimensional culture and in vivo human epidermis, the majority of suprabasal cells were CTRB2+ cells, in spite of their non-proliferative Ki-67− nature. The tumor mass of BD and SCC contained CTRB1+ cells and Ki-67+ proliferating and Ki-67− non-proliferative CTRB2+ cells. Clumping cells in BD had increased numbers of centrioles, with an approximate 1:1 to 2:1 ratio of centrobin+ to ODF2+ centrioles. Conclusions: The cell cycle arrest of suprabasal cells is distinct from the G0 arrest of monolayered epithelial cells. Tumor mass of BD and SCC contained non-proliferative cells with the characteristics of the suprabasal cells of normal epidermis. A constant ratio of the number of centrobin+ to ODF2+ centrioles indicates that multiple centrioles were induced by cell division failure rather than centriole overduplication in clumping cells.

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Papers, etc., Registered in KOARA 【 Display / hide

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Reviews, Commentaries, etc. 【 Display / hide

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Presentations 【 Display / hide

  • 免疫チェックポイント阻害薬抵抗の進行期悪性黒色腫に対する殺細胞性抗癌剤の治療効果

    AMAGAI MASAYUKI

    第881回日本皮膚科学会東京地方会 (東京) , 2018.09, Oral Presentation(general)

  • 透析患者においてセクキヌマブが有効であった尋常性乾癬・関節症性乾癬の3例

    AMAGAI MASAYUKI

    第33回日本乾癬学会学術大会 (愛媛) , 2018.09, Oral Presentation(general)

  • 類天疱瘡を合併した尋常性乾癬の3例

    AMAGAI MASAYUKI

    第33回日本乾癬学会学術大会 (愛媛) , 2018.09, Oral Presentation(general)

  • アトピー性皮膚炎患者と健常人の皮膚由来黄色ブドウ球菌株の解析

    AMAGAI MASAYUKI

    第63回日本ブドウ球菌研究会 (鹿児島) , 2018.08, Oral Presentation(general)

  • NCSTN変異を同定したfamilial acne inversaの姉妹例

    AMAGAI MASAYUKI

    第880回日本皮膚科学会東京地方会 (東京) , 2018.07, Oral Presentation(general)

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Research Projects of Competitive Funds, etc. 【 Display / hide

  • 皮膚細菌叢と宿主の相互作用理解に基づく炎症性疾患制御法の開発

    2016.10
    -
    2022.03

    日本医療研究開発機構(AMED)CREST, Principal Investigator

  • 皮膚・腸内微生物叢解析によるアトピー性皮膚炎発症機序の解明

    2016.04
    -
    2019.03

    日本医療研究開発機構(AMED), Principal Investigator

  • ステロイド治療抵抗性の天疱瘡患者を対象としたリツキシマブの医師主導治験

    2017.04
    -
    2020.03

    日本医療研究開発機構(AMED), Principal Investigator

  • 稀少難治性皮膚疾患に関する調査研究

    2017.04
    -
    2020.03

    Health and Labour Sciences Research Grants, Principal Investigator

  • ガイドライン最適化を目的とした自己免疫性水疱症に対する抗CD20抗体療法の評価

    2015.04
    -
    2017.03

    日本医療研究開発機構(AMED), Principal Investigator

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Works 【 Display / hide

  • 河北新聞 朝刊 15面「皮膚にぺたり「極薄」電極」

    2017.09

    Other, Joint

  • 読売新聞 朝刊 25面「肌に貼れる電子回路 スポーツ・医療で応用」

    2017.08

    Other, Joint

  • 日本経済新聞 朝刊 9面「皮膚に貼り付けるシート状電極開発」

    2017.07

    Other, Joint

  • 薬事日報 朝刊 8面「極薄ナノメッシュセンサー開発 長期生体計測への応用に期待」

    2017.07

    Other, Joint

  • フジサンケイビジネスアイ 朝刊 11面「皮膚に水で貼り付け長期測定 JSTなど超軽量ナノメッシュセンサー開発」

    2017.07

    Other, Joint

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Intellectual Property Rights, etc. 【 Display / hide

  • 自然発症皮膚炎の新規原因因子及び皮膚疾患モデル動物

    Application No.: 特願 2012-047521  2012.03 

    Announcement No.: 特開2013-179920  2013.09 

    Registration No.: 特許第5959235号  2016.07

    Patent, Joint

  • 毛乳頭細胞の培養方法

    Application No.: PCT/JP2009/063920  2009.08 

    Announcement No.: WO2010/021245  2010.02 

    Patent, Joint

  • アレルギー疾患モデル動物

    Application No.: 特願2010-511897  2009.05 

    Announcement No.: WO2009/139191  2009.11 

    Registration No.: 特許第5606907号  2014.09

    Patent, Joint

  • Allergic Disease Model Animals

    Application No.: PCT/JP2009/002161  2009.05 

    Announcement No.: WO2009/139191  2009.11 

    Registration No.: US8350118  2013.01

    Patent, Joint

  • Drug Delivery to Human Tissues by Single Chain Variable Region Antibody Fragments Cloned by Phage Display

    Application No.: PCT/US2008/00288  2008.01 

    Announcement No.: WO/2008/085987  2008.07 

    Registration No.: US2011/0200601  2011.08

    Patent, Joint

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Awards 【 Display / hide

  • 皆見省吾記念賞

    1990.04, 日本皮膚科学会, Partial cDNA cloning of the 230 ‐ kD mouse bullous pem- phigoid antigen by use of a human monoclonal antibase- mentmembrane zone antibody.

    Type of Award: Awards of National Conference, Council and Symposium

  • JSID賞

    AMAGAI MASAYUKI, 2000.09, 日本研究皮膚科学会

    Type of Award: Awards of National Conference, Council and Symposium

  • Alfred Marchionini Research Award

    Amagai Masayuki, 2002.07, World Congress of Dermatology, 自己免疫性疾患、天疱瘡の病態解明に関する一連の卓越した業績に対して贈られた

    Type of Award: International Academic Awards

  • Morris H Samitz Lectureship Award

    2002.11, University of Pennsylvania

    Type of Award: Other Awards

  • William Montagna Lectureship Award

    AMAGAI MASAYUKI, 2003.05, The Society for Investigative Dermatology, Pemphigus: A simple logic behind a complex disease

    Type of Award: International Academic Awards

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Courses Taught 【 Display / hide

  • DERMATOLOGY: PRACTICE

    2020

  • DERMATOLOGY

    2020

  • CLINICAL ONCOLOGY: SEMINAR

    2020

  • CLINICAL ONCOLOGY: PRACTICE

    2020

  • ADVANCED DERMATOLOGY

    2020

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Courses Previously Taught 【 Display / hide

  • 免疫学講義「皮膚免疫」

    Keio University, 2017, Lecture

  • 大学院生主科目講義 医学特別講義「Skin as an immune organ」

    Keio University, 2017, Lecture

  • 皮膚科学講義「皮膚疾患の診断と治療・皮膚科学の今後の展望」

    Keio University, 2017, Lecture, Within own faculty

  • 皮膚科学講義「皮膚科学総論・皮疹の診方」

    Keio University, 2017, Lecture, Within own faculty

  • 免疫学講義「皮膚免疫」

    Keio University, 2016, Lecture

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Social Activities 【 Display / hide

  • 内閣府 日本学術会議 会員

    2017.10
    -
    2023.09
  • 内閣府 日本学術会議 連携会員

    2006.08
    -
    2017.09
  • 厚生科学審議会疾病対策部会 リウマチ・アレルギー対策委員会  アレルギー疾患対策作業班委員

    2011.01
    -
    2012.03
  • 日本学術振興会 学術システム研究センター研究員

    2010.04
    -
    2013.03
  • 厚生労働省 難治性疾患克服研究評価委員会 小委員会委員

    2010.02
    -
    2012.02

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Memberships in Academic Societies 【 Display / hide

  • National Academy of Medicine

     
  • 日本皮膚科学会

     
  • 日本研究皮膚科学会

     
  • 日本臨床皮膚科医会

     
  • 日本細胞生物学会

     

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