Elucidation of the action of uric acid and its molecular mechanism in psoriasis based on animal models

2023 Fiscal Year Final Research Report

• Project/Area Number: 21K16217
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 53050:Dermatology-related
• Research Institution: Teikyo University
• Principal Investigator: Kimura Yoshitaka 帝京大学, 医学部, 助教 (90807843)
• Project Period (FY): 2021-04-01 – 2024-03-31
• Keywords: 尿酸 / 乾癬 / 炎症

Outline of Final Research Achievements

In hypouricemic mice, the severity of skin lesions like psoriasis induced by imiquimod, was significantly suppressed clinically and pathologically, indicating that uric acid exaggerates psoriatic inflammation. The infiltration of IL-17 producing T cells into lesions was suppressed in hypouricemic mice; in contrast, the number of cells in the lymph nodes and spleen did not differ. Furthermore, chemokine expression in skin lesions decreased in hypouricemic mice and in vitro chemokine expression in keratinocytes increased in the presence of uric acid. These results show that uric acid promotes chemokine expression in the epidermis, which causes exaggerated psoriatic inflammation.

Free Research Field

自然免疫

Academic Significance and Societal Importance of the Research Achievements

乾癬に高頻度に合併する高尿酸血症が、表皮のターンオーバーの結果として生じる単なる併存疾患でなく、乾癬病態自体に関与している可能性を示した。乾癬患者における高尿酸血症のコントロールの重要性を示すとともに、尿酸および尿酸が関与する分子をターゲットとする新しい乾癬の治療方法の開発などに有用である。