The mechanism of adenosine diphosphate receptor mediated thrombus formation in antiphospholipid syndrome.

2014 Fiscal Year Final Research Report

• Project/Area Number: 25670455
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Collagenous pathology/Allergology
• Research Institution: Hokkaido University
• Principal Investigator: ATSUMI Tatsuya 北海道大学, 医学(系)研究科(研究院), 教授 (20301905)
• Co-Investigator(Kenkyū-buntansha): OKU Kenji 北海道大学, 北海道大学病院, 助教 (70544295)
• Project Period (FY): 2013-04-01 – 2015-03-31
• Keywords: 抗リン脂質抗体 / 血小板 / アデノシン2リン酸（ADP）

Outline of Final Research Achievements

With any of the subtypes of 231D, a mouse monoclonal antiphospholipid antibody, dysfunction of adenosine diphosphate (ADP) induced platelet aggregation was not detected in a reproducible manner. By contrast, EY2C9, a human monoclonal antiphospholipid antibody or purified IgG from sera of antiphospholipid syndrome(APS) patients induced suppression of ADP triggered platelet aggregation. The mechanism of the phenomena is under analysis.
In flow-analysis with the micro-tip mimicked sclerotic-artery, monoclonal antiphospholipid antibody did not show the decisive tendency of creating white blood clot. Inhibitor of P2Y12, the major ADP receptor on the platelet membrane, is widely used for the prophylaxis of thrombosis in patients with the history of arterial thrombosis including APS patients. However, our data suggest that there may be certain amount of patients in APS that the ADP inhibitor is not effective enough for preventing the recurrent thrombosis.

Free Research Field

膠原病・リウマチ学