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血小板整合素 α2β1 密度的遗传变异性:可能是导致间日疟原虫引起严重血小板减少症的原因之一。

Genetic variability in platelet integrin α2β1 density: possible contributor to Plasmodium vivax-induced severe thrombocytopenia.

机构信息

Centro de Pesquisas René Rachou, Fundação Oswaldo Cruz, Belo Horizonte, Minas Gerais, Brazil.

出版信息

Am J Trop Med Hyg. 2013 Feb;88(2):325-8. doi: 10.4269/ajtmh.2012.12-0297. Epub 2012 Dec 18.

Abstract

Understanding the pathogenesis of Plasmodium vivax malaria is challenging. We hypothesized that susceptibility to P. vivax-induced thrombocytopenia could be associated with polymorphisms on relevant platelet membrane integrins: integrin α2 (C807T), and integrin β3 (T1565C). Although β3 polymorphism was not related with P. vivax malaria, α2 807T carriers, which show high levels of integrin α2β1, had a higher probability for severe thrombocytopenia than wild-type carriers. This evidence of the association of integrin polymorphism and P. vivax morbidity was further demonstrated by a moderate but significant correlation between clinical disease and surface levels of the integrin α2β1.

摘要

理解间日疟原虫疟疾的发病机制具有挑战性。我们假设对间日疟原虫诱导的血小板减少症的易感性可能与相关血小板膜整合素的多态性有关:整合素 α2(C807T)和整合素 β3(T1565C)。尽管 β3 多态性与间日疟原虫疟疾无关,但高表达整合素 α2β1 的 α2 807T 携带者发生严重血小板减少症的可能性高于野生型携带者。整合素多态性与间日疟原虫发病率之间的关联的证据进一步通过整合素 α2β1 的临床疾病与表面水平之间的中度但显著的相关性得到证明。

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