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骨髄細胞によって分泌されるIL-23は,カストレーションに抵抗する前立腺がんを誘発する

Arianna Calcinotto¹, Clarissa Spataro¹, Elena Zagato¹

¹Institute of Oncology Research (IOR), Oncology Institute of Southern Switzerland, Bellinzona, Switzerland.

|June 29, 2018

まとめ

ミエロイド由来抑制細胞 (MDSC) は,IL-23を産生することで,カストレーション抵抗性前立腺がん (CRPC) を駆動する. IL-23を阻害することで,アンドロゲン欠乏療法に対する感受性を回復させ,CRPCに対する新しい治療戦略を提供することができる.

科学分野:

腫瘍学
免疫学
癌生物学

背景:

前立腺がんはしばしばアンドロゲン欠乏療法に抵抗し,カストレーション抵抗性前立腺がん (CRPC) に進行する.
腫瘍の微小環境は癌の進行と治療への抵抗に重要な役割を果たします
CRPCを駆動するメカニズムの理解は効果的な治療法の開発に不可欠です

研究の目的:

腫瘍の微小環境が排泄に抵抗する前立腺がんの発生に与える影響を調べる
CRPCを促進するマイクロ環境によって生み出される特定の要因を特定する.
これらの要因を標的とした潜在的な治療戦略を探求する.

主な方法:

CRPC患者とマウスの腫瘍サンプルと血液の分析
骨髄由来抑制細胞 (MDSC) によって生成されるサイトカインの識別.
CRPCのマウスモデルでの抗体媒介によるIL-23の不活性化を用いたin vivo実験.

主要な成果:

MDSCsによって生成されるインタールイキン-23 (IL-23) は,CRPCの主要な要因として特定されました.
IL-23は前立腺腫瘍細胞におけるアンドロゲン受容体経路を活性化させ,アンドロゲン欠乏状態での生存と増殖を促進する.
CRPC患者では,MDSC浸透とIL-23濃度の上昇が観察されました.
アンドロゲン欠乏療法に対する感受性を回復させた.

結論:

MDSCは,IL-23を分泌することによって,非細胞自律的メカニズムを通じてCRPCを促進する.
前立腺がんにおけるMDSC媒介によるカストレーション抵抗を克服するための有望な治療戦略です.
IL - 23 阻害は,標準的な前立腺がん治療と連携する可能性があります.

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