慢性骨髓增殖性疾病中骨髓细胞黏附因子CD239的表达

Expression of adhesion factor CD239 in bone marrow cells in chronic myeloproliferative diseases.

作者信息

Hussein Kais, Theophile Katharina, Denzer Katrin, Kreipe Hans, Bock Oliver

机构信息

Institute of Pathology, Hannover Medical School, Carl-Neuberg-Strasse 1, Hannover, Germany.

出版信息

J Thromb Thrombolysis. 2009 Oct;28(3):299-303. doi: 10.1007/s11239-008-0285-z. Epub 2008 Oct 30.

DOI:10.1007/s11239-008-0285-z

PMID:18972067

Abstract

Patients suffering from Philadelphia chromosome-negative chronic myeloproliferative disease (Ph(-) CMPD), such as polycythaemia vera (PV), are frequently JAK2(V617F)-mutated and have an elevated risk for thromboembolic complications. Recent data indicated that the molecular basis of JAK2(V617F) and thrombosis might be related to increased expression of CD239, the Lutheran blood group/basal cell adhesion molecule, in PV-derived red blood cells. The aim of this study was to clarify whether JAK2(V617F) PV with thromboembolism is characterised by CD239 overexpression. Leukocyte-derived JAK2(V617F) was detectable in bone marrow cells but also in liver and spleen explants and transplants after thrombosis (95% JAK2(V617F)-positive Ph(-) CMPD, n = 66). CD239 was expressed in a constitutive fashion in PV-derived bone marrow cells and thus a pro-thrombotic function does not seem to be mediated by increased CD239 expression alone.

摘要

患有费城染色体阴性慢性骨髓增殖性疾病（Ph(-) CMPD）的患者，如真性红细胞增多症（PV），经常发生JAK2(V617F)突变，并且有血栓栓塞并发症的风险升高。最近的数据表明，JAK2(V617F)与血栓形成的分子基础可能与PV来源的红细胞中CD239（路德血型/基底细胞粘附分子）表达增加有关。本研究的目的是阐明伴有血栓栓塞的JAK2(V617F) PV是否以CD239过表达为特征。血栓形成后，在骨髓细胞中可检测到白细胞来源的JAK2(V617F)，在肝脏和脾脏外植体及移植组织中也可检测到（95% JAK2(V617F)阳性的Ph(-) CMPD，n = 66）。CD239在PV来源的骨髓细胞中以组成性方式表达，因此促血栓形成功能似乎并非仅由CD239表达增加介导。