Oda A, Ochs H D
Hokkaido Red Cross Blood Center, Sapporo, Japan.
Immunol Rev. 2000 Dec;178:111-7. doi: 10.1034/j.1600-065x.2000.17808.x.
Wiskott-Aldrich syndrome (WAS) and X-linked thrombocy topenia (XLT) are caused by mutations of the WAS protein (WASP) gene. The manifestations of the classic WAS phenotype consist of immunodeficiency, eczema and thrombocytopenia. However, thrombocytopenia and small platelets are the only consistent features of WAS and XLT. The exact mechanisms of the development of thrombocytopenia in patients with WAS or XLT are unknown. To date, platelets are the only primary cells in which inducible tyrosine phosphorylation of WASP has been consistently demonstrated. This review focuses on the recent progress in dissecting the causes of thrombocytopenia and the emerging understanding of WASP phosphorylation.
威斯科特-奥尔德里奇综合征(WAS)和X连锁血小板减少症(XLT)是由WAS蛋白(WASP)基因突变引起的。经典WAS表型的表现包括免疫缺陷、湿疹和血小板减少。然而,血小板减少和小血小板是WAS和XLT仅有的一致特征。WAS或XLT患者血小板减少发生的确切机制尚不清楚。迄今为止,血小板是唯一一直被证实可诱导WASP酪氨酸磷酸化的原代细胞。本综述重点关注在剖析血小板减少病因方面的最新进展以及对WASP磷酸化的新认识。