原发免疫性血小板减少症（ITP）是一种自身免疫功能异常导致的血小板减少综合征。去唾液酸化是血小板破坏的重要途径，我们在前期研究中发现ITP患者血小板去唾液酸化水平显著升高，伴有血清唾液酸酶浓度和活性增加，唾液酸酶抑制剂表现出对ITP的治疗价值，提示去唾液酸化介导的血小板破坏有可能在ITP的发病中起到重要作用。CD8+T细胞可直接杀伤血小板，但其相对较少的数量可能不足以解释ITP中大量血小板破坏。我们推测CD8+T细胞介导的血小板破坏可能引起血小板内唾液酸酶释放，催化外周血小板去唾液酸化进而在肝内破坏。本研究拟通过体外细胞培养和主动型ITP小鼠模型，从细胞和分子水平揭示去唾液酸化在ITP发病中的作用以及机制，并探索特异性阻断去唾液酸化对ITP可能具有的治疗价值，为临床诊疗提供新的思路。

Primary immune thrombocytopenia (ITP) is an autoimmune abnormality- conducted thrombocytopenic syndrome. Desialylation has been proven to be an essential approach in platelet destruction. Our previous investigation prompted a significantly up-regulation in platelet surface glycoprotein desialylation level accompanied by increase of serum sialidase concentration and activity. Sialidase inhibitor, such as Oseltamivir and DANA, shows potential therapeutic value to ITP. All above indicates that desialylation-mediated platelet destruction is probably involved in ITP pathogenesis. Cytotoxic CD8+ T cell-mediated platelet lysis attributes to thrombocytopenia in ITP, though it is argued that the minor CD8+ T cell subset could not account for the numerous platelet destruction. Hereby we propose that platelet lysis mediated by CD8+ T cell would release sialidase residing in granules within platelet and desialyte circulating platelet that finally destroyed in liver. This research aims at demonstrating the roles and mechanisms of desialylation in ITP pathogenesis, and discovering the potential therapeutic value to specifically blockade platelet desialylation.