Nagahama Minori, Nomura Shosaku, Kanazawa Shigenori, Ozaki Yoshio, Kagawa Hideo, Fukuhara Shirou
First Department of Internal Medicine, Kansai Medical University, Osaka Japan.
Eur J Haematol. 2002 Nov-Dec;69(5-6):303-8. doi: 10.1034/j.1600-0609.2002.02774.x.
We investigated the levels of various chemokines and soluble CD40L (sCD40L) in ITP patients, in order to determine the influence of CD40-CD40L interaction on the pathogenesis of ITP. We found increases in MCP-1 and RANTES levels in ITP patients compared with those in healthy individuals. Thirty-eight of the 65 ITP patients (58.5%) had elevated levels of sCD40L. We found significant decreases in platelet counts in sCD40L-positive ITP patients. Although the sCD40L level did not differ significantly between the control and nonimmune thrombocytopenia groups, but among ITP patients. sCD40L level was significantly higher in those with untreated ITP than in those with treated ITP. In addition, significant increases in RANTES, MCP-1, sCD14, and sP-selectin levels were observed in sCD40L-positive ITP patients, although sE-selectin levels were not increased in such patients. For other factors examined, however, there were no differences in level between sCD40L-positive and -negative ITP patients. These findings suggests that there are two groups of ITP patients, one with elevated and one with normal of sCD40L. ITP cases in which sCD40L was increased appeared to involve changes in platelet counts and monocyte activation. The pathogenesis of ITP may in some patients include alterations of the CD40/CD40L pathway.
我们研究了免疫性血小板减少症(ITP)患者体内各种趋化因子和可溶性CD40配体(sCD40L)的水平,以确定CD40 - CD40L相互作用对ITP发病机制的影响。我们发现,与健康个体相比,ITP患者的单核细胞趋化蛋白-1(MCP - 1)和调节激活正常T细胞表达和分泌因子(RANTES)水平升高。65例ITP患者中有38例(58.5%)的sCD40L水平升高。我们发现sCD40L阳性的ITP患者血小板计数显著降低。虽然对照组和非免疫性血小板减少症组之间的sCD40L水平无显著差异,但在ITP患者中,未治疗的ITP患者的sCD40L水平显著高于接受治疗的患者。此外,sCD40L阳性的ITP患者中,RANTES、MCP - 1、可溶性CD14(sCD14)和可溶性P选择素(sP - 选择素)水平显著升高,不过此类患者的可溶性E选择素(sE - 选择素)水平并未升高。然而,对于其他检测因素,sCD40L阳性和阴性的ITP患者之间水平并无差异。这些发现表明存在两组ITP患者,一组sCD40L水平升高,另一组正常。sCD40L升高的ITP病例似乎涉及血小板计数变化和单核细胞激活。ITP的发病机制在一些患者中可能包括CD40/CD40L途径的改变。