Department of Hematology, Faculty of Medicine, Eskisehir Osmangazi University , Eskiehir 26480 Turkey.
Platelets. 2013;24(8):625-31. doi: 10.3109/09537104.2012.748188. Epub 2012 Dec 7.
Primer immunologic defect in patients with idiopathic thrombocytopaenic purpura (ITP) result from autoreactive B-lymphocytes secreting antiplatelet antibodies. Dysfunctional cellular immunity has also great importance in ITP pathogenesis. CD4(+)CD25(+) regulatory T-cells have immunoregulatory features and it is able to inhibit CD4(+)CD25(-) and CD8(+) responses. ITP is also an autoimmune disease; the CD4(+)CD25(+) T-cell levels of the patients decrease during the active state. According to our findings, immunosuppressive treatments increase the CD4(+)CD25(+) Treg cell levels in the non-remission ITP patients. However, this level is not enough to overcome the resistance. CD4(+)CD25(-)Foxp3(+) and CD4(+)Foxp3(+) Treg cells are responsible for the pathogenesis of the non-remission ITP patients and other factors exist, which are responsible for the resistance of ITP treatment.
特发性血小板减少性紫癜(ITP)患者的原发性免疫缺陷是由于自身反应性 B 淋巴细胞分泌抗血小板抗体所致。细胞免疫功能障碍在 ITP 的发病机制中也具有重要意义。CD4+CD25+调节性 T 细胞具有免疫调节功能,能够抑制 CD4+CD25-和 CD8+反应。ITP 也是一种自身免疫性疾病;在活动期,患者的 CD4+CD25+T 细胞水平下降。根据我们的发现,免疫抑制治疗可增加非缓解 ITP 患者的 CD4+CD25+Treg 细胞水平。然而,这一水平还不足以克服耐药性。CD4+CD25-Foxp3+和 CD4+Foxp3+Treg 细胞是导致非缓解 ITP 患者发病的原因,此外还存在其他导致 ITP 治疗耐药的因素。