感染人?微小病毒B19 的症?與抗磷脂質症候群(anti-phospholipid
syndrome; APS) 相似，?如抗磷脂質抗體產生、血栓和血小板減少
等。文獻已知抗磷脂質症候群的致病機制為抗磷脂質抗體與Glycoprotein I(GPI)蛋白作用結合至內皮細胞，活化細胞黏附因子進而導致發炎和凝血現象產生。近幾?實驗室發現B19-VP1u 抗體具有抗磷脂質抗體?似的功能，可活化血管內皮細胞黏附因子及透過被動免疫模式引發小鼠凝血時間延長與血小板減少等?似抗磷脂質症候群症?的產生。然而最近有文獻另探討抗磷脂質抗體具有促進血管新生(angiogenesis)的功能。因此我們想?解B19 抗體對血管新生的角色。我們將B19 抗體與人?臍靜脈內皮細胞共同培養，?用西方墨點法分析細胞蛋白質表現，研究結果發現B19 抗體與抗磷脂質抗體對臍靜脈內皮細胞的細胞存活沒有明顯影響，?會促進細胞黏附因子和細胞整合素的表現。但是在血管新生訊息傳遞?徑則明顯發現抗磷脂質抗體會促進AKT-mTOR-S6RP 活化?徑，而B19 抗體則沒有顯著影響。因此這些發現提供??多訊息有關B19 抗體在血管新生調節作用的角色。The symptom of human parvovirus B19 infection is similar to
anti-phospholipid syndrome (APS) such as the anti-phospholipid antibody production, thrombosis and thrombocytopenia. In previous study have shown
that the pathogenesis of APS is the anti-phospholipid antibody interacting with Glycoprotein I (GPI) and binding to endothelial cell, which up-regulate adhesion molecular that lead to vasculopathy and blood clotting.
In recent years, our Lab found that anti-B19-VP1u antibody has the similar function with anti-phospholipid antibody, which does activate vascular endothelial cell and induce adhesion molecular and cause APS-like symptom by passive immunization that include prolonged aPTT and thrombocytopenia.However, recent study described that antibody against phospholipid can promote angiogenesis. Therefore, we would like to further understand the
role of B19 antibody in angiogenesis. We incubated HUVEC endothelial cell with various B19 antibodies and analysis protein expression by Western blot. The results indicated that B19 antibody do not affect cell survival rate
significantly but can up-regulate the expression of adhesion molecular. The anti-phospholipid antibody lead to angiogenesis via AKT-mTOR-S6RP pathway, but B19 antibody does not. Therefore, these findings provide further information concerning the role of B19 antibodies are not involved in regulate angiogenesis.
