Role of lysophosphatidylserine-producing enzyme (PS-PLA1) in the pathogenesis of SLE and further applications as SLE biomarker

• Project/Area Number: 25461487
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Collagenous pathology/Allergology
• Research Institution: Tokyo Medical University
• Principal Investigator: Sawada Tetsuji 東京医科大学, 医学部, 准教授 (50235470)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Project Status: Completed (Fiscal Year 2015)
• Budget Amount: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000); Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000); Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000); Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
• Keywords: 全身性エリテマトーデス / リゾリン脂質

Outline of Final Research Achievements

We determined the serum levels of lysophosphatidic acid-producing enzyme (ATX) and lysophosphatidylserine-producing enzyme (PS-PLA1) to clarify the role of the lysophospholipid in the pathophysiology SLE. The serum level of PS-PLA1 was significantly higher in SLE patients, and correlated with some of the SLE disease activity indices. In pristine-induced mouse SLE model, PS-PLA1 positive cells were more frequently detected in spleen. T cell stimulation led to the increase of PS-PLA1 expression and decrease of LPS receptor expression. High concentration of IFN-α increased the PS-PLA1 expression in peripheral blood mononuclear cells. Therefore, PS-PLA1 is considered to be a T-cell activation marker as well as a member of IFN-α signatures.