发病机制
免疫学
免疫系统
免疫
医学
体液免疫
细胞免疫
获得性免疫系统
免疫性血小板减少症
生物
血小板
作者
Yufeng Yuan,Yang Xiang,Yi-Jian Chen
出处
期刊:PubMed
日期:2019-10-01
卷期号:27 (5): 1706-1710
标识
DOI:10.19746/j.cnki.issn.1009-2137.2019.05.054
摘要
Abstract Immune thrombocytopenia (ITP) is a complex autoimmune disease characterized by less than 100×109/L platelet count in peripheral blood. The pathogenesis of ITP is complex and has not been fully elucidated. Currently, researches on the pathogenesis of ITP mainly focus on the disorders of humoral immunity and cellular immunity. In recent years, some new progress has been made in the study of this pathogenesis, including the platelet clearance pathway that is not dependent on Fc γ R mediation, the metalloproteinase (ADAM) 10 that can regulate T and B cells, and the abnormal expression of micro RNA in genetic factors. Under the joint action of multiple factors, the imbalance of the immune system in the body leads to the occurrence of ITP. This article reviews the research progress on humoral immunity, cellular immunity and other possible new pathogenesis of ITP in recent years.原发性免疫性血小板减少症的发病机制研究进展.原发性免疫性血小板减少症(Immune thrombocytopenia,ITP)是一种复杂的自身免疫疾病,以外周血中血小板计数<100×109/L为特点。ITP的发病机制复杂,尚未完全阐明,目前对ITP发病的研究主要针对于体液免疫失调以及细胞免疫失调等方面。近年来,研究该发病机制取得了一些新的进展,包括非依赖Fc γ R 介导的血小板清除途径,可以调节T、B细胞的金属蛋白酶(ADAM)10,遗传因素中的微小RNA的表达异常等。在多种因素的共同作用下,机体免疫系统的失衡,导致ITP的发生。本文就近年来针对ITP研究的体液免疫,细胞免疫以及其他可能的新发病机制研究进展进行综述。.
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