2022 Fiscal Year Final Research Report
Role of Th17 cell expansion through CCR4 in psoriasis
| Project/Area Number |
20K08700
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 53050:Dermatology-related
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| Research Institution | Kindai University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
松尾 一彦 近畿大学, 薬学部, 講師 (70615921)
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| Project Period (FY) |
2020-04-01 – 2023-03-31
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| Keywords | 乾癬 / CCR4 / Th17 |
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| Outline of Final Research Achievements |
In the present study, we examined the role of CCR4 in psoriasis. CCR4 deficiency caused the decrease in skin disease and expression levels of psoriasis-related genes. Furthermore, Th17 cells were reduced in the skin lesions and regional lymph
nodes of CCR4 deficient mice. In the regional lymph nodes, CCR4-positive Th17 cells were clustered with CCL22-producing dendritic cells, and these clusters were decreased in CCR4 deficient mice. Similar results were observed in selective CCR4 antagonist-treated mice. These findings suggest that CCR4 would be involved in the pathology of psoriasis through the expansion of Th17 cells in the lymph nodes.
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| Free Research Field |
免疫学
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| Academic Significance and Societal Importance of the Research Achievements |
乾癬は、自己免疫性疾患の1つであり、未だ根本的な治療法が無い。Th17細胞が関連すると言われているが、その寄与の詳細は不明である。また、CCR4は、Th2細胞やTh17細胞に発現しており、これまでアレルギーなどのTh2疾患において重要な役割を果たすことが報告されているが、Th17疾患への寄与は不明であった。本研究で明らかにした、CCR4が所属リンパ節でのTh17細胞増殖を介して、乾癬の増悪に寄与するという知見は、乾癬の病態解明に貢献すると考えている。CCR4を標的とした乾癬の新たな治療戦略の開発に繋がることが期待される。
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