@techreport{oai:kindai.repo.nii.ac.jp:00021452,
 author = {中山, 隆志 and 松尾, 一彦},
 month = {},
 note = {https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-17K10217/, 研究成果の概要（和文）：本研究において研究代表者は、ケモカインELC/CCL19がGPCR#13受容体の新規の機能的リガンドであることを見出した。また、ELC/CCL19はGPCR#13に対して、既知受容体のCCR7と同程度のアゴニスト活性を持ち、CCR7を発現していないGPCR#13陽性のエフェクター細胞の遊走を担う機能的なリガンドであることを明らかにした。また、乾癬モデルマウスへのELC/CCL19の経皮投与により、病変部でのGPCR#13陽性エフェクター細胞の浸潤が増加し、乾癬病態が増悪した。以上の結果より、ELC/CCL19-GPCR#13系が乾癬の病態形成に重要な役割を果たしている可能性が示された。研究成果の概要（英文）：ELC/CCL19 is a functional ligand for CCR7, which is mainly expressed by naive T and B cells. In the present study, we found that ELC/CCL19 is also a functional ligand for GPCR#13, which is broadly expressed by effector cells such as NK cells and monocytes. We revealed that ELC/CCL19 efficiently induced cell migration in murine L1.2 cells stably expressing GPCR#13 (L1.2-GPCR#13) as well as in L1.2-CCR7. Furthermore, In chemotaxis assays using human PBMCs, ELC/CCL19 attracted not only naive T cells but also CD16(+) NK cells and CD14(+) monocytes. In addition, ELC/CCL19-mediated cell migration was suppressed by treatment with a GPCR#13 antagonist. In mouse psoriasis model, intradermal injection of ELC/CCL19 recruited GPCR#13(+)/CCR7(-) effector cells in psoriasis-like skin lesions and exacerbated psoriasis-like inflammation. These results suggest that ELC/CCL19 another agonist for GPCR#13 and may play an important role in psoriasis by recruiting GPCR#13-expressing effector cells., 研究種目：基盤研究(C);  研究期間：2017～2019;   課題番号：17K10217;   研究分野：免疫学;   科研費の分科・細目：, application/pdf},
 title = {ケモカインＥＬＣ／ＣＣＬ１９の新規受容体同定とその乾癬における役割の解明},
 year = {2020},
 yomi = {ナカヤマ, タカシ and マツオ, カズヒコ}
}