難治性多発性骨髄腫のヒト化抗CD26モノクローナル抗体を用いた分子標的療法の開発

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Author: 西田, 浩子ほか

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Publication date: 2019

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Note (General)：: type:textヒト破骨細胞にはCD26が機能的に発現し、多発性骨髄腫患者骨髄では、破骨細胞・血管内皮細胞近傍にCD26陽性骨髄腫細胞が存在する。破骨細胞との共存により骨髄腫細胞のCD26発現は増強し、ヒト化抗CD26モノクローナル抗体は、破骨前駆細胞より破骨細胞への分化を抑制するとともに、CD2...

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Material Type: 文書・図像類
Title: 難治性多発性骨髄腫のヒト化抗CD26モノクローナル抗体を用いた分子標的療法の開発
Author/Editor: 西田, 浩子
山田, 健人
Author Heading: 西田, 浩子
山田, 健人
Publication Date: 2019
Publication Date (W3CDTF): 2019
Alternative Title: ナンチセイタハツセイコツズイシュノヒトカコウCD26 モノクローナルコウタイオモチイタブンシヒョウテキリョウホウノカイハツ
Nanchisei tahatsusei kotsuzuishu no hitoka kōCD26 monokurōnaru kōtai o mochiita bunshi hyōteki ryōhō no kaihatsu
Molecular-targeted therapy by humanized anti-CD26 monoclonal antibody in relapsed or refractory multiple myeloma
Periodical title: 科学研究費補助金研究成果報告書
Text Language Code: jpn
eng
Subject Heading: CD26,破骨細胞,ヒト化抗CD26モノクローナル抗体,多発性骨髄腫,ADCC,新規薬剤,SP細胞,骨髄微小環境
Target Audience: 一般
Note (General): type:text
ヒト破骨細胞にはCD26が機能的に発現し、多発性骨髄腫患者骨髄では、破骨細胞・血管内皮細胞近傍にCD26陽性骨髄腫細胞が存在する。破骨細胞との共存により骨髄腫細胞のCD26発現は増強し、ヒト化抗CD26モノクローナル抗体は、破骨前駆細胞より破骨細胞への分化を抑制するとともに、CD26陽性骨髄腫細胞に対し、抗体依存性細胞障害活性(ADCC)及び直接的効果を通じ、抗腫瘍効果を呈する。更に、免疫調整薬と抗CD26体投与の併用は、そのADCC活性を相乗的に増強し、抗体は、生体内でのヒト骨髄における骨髄腫細胞増殖および破骨細胞形成の双方を抑制し、難治性骨髄腫の新規治療法として有用な治療戦略となりうる。 Recently, we identified CD26 expression on human osteoclasts (OCs) and demonstrated that humanized anti-CD26 monoclonal antibody (huCD26mAb) inhibits human OC differentiation. We showed that CD26 expression was present on plasma cells in the bone marrow tissues of multiple myeloma (MM) patients. In vitro immunostaining studies revealed that although CD26 expression was low or absent on MM cell lines cultured alone, it was intensely and uniformly expressed on myeloma cell lines co-cultured with OCs. The augmented CD26 expression in MM cells was exploited to enhance anti-MM efficacy of huCD26mAb via a substantial increase in antibody-dependent cytotoxicity (ADCC). Moreover, huCD26mAb in combination with novel agents synergistically enhanced huCD26mAb induced ADCC activity against CD26+ MM cells, compared with each agent alone. huCD26mAb significantly reduced the MM tumor burden and OC formation in vivo. These results suggest that huCD26mAb could act as a therapeutic agent in MM.
研究種目 : 基盤研究 (C) (一般) 研究期間 : 2016～2019 課題番号 : 16K07180 研究分野 : 血液内科学、腫瘍治療学
Access Restrictions: 限定公開
Related Material: 科研費研究者番号 : 80317130
科研費研究者番号 : 60230463
Data Provider (Database): 国立情報学研究所 : 学術機関リポジトリデータベース（IRDB）（機関リポジトリ）
https://irdb.nii.ac.jp
Original Data Provider (Database): 慶應義塾大学 : 慶應義塾大学学術情報リポジトリ