特发性血小板减少性紫癜患者外周血共刺激分子的表达及与血小板抗体关系的临床研究

Expression of Co-stimulatory Molecules in Peripheral Blood of Patients with Idiopathic Thrombocytopenic Purpura in Relation with Platelet Antibodies

本研究检测特发性血小板减少性紫癜(ITP)患者外周血共刺激分子CD80、CD86和CD137的表达及血清血小板抗体(PAIgG)含量并探讨二者相关性及与血小板数量等疾病表现的关系,以期阐明共刺激分子在特发性血小板减少性紫癜发病及病情判断中的作用。分别应用免疫荧光法和流式细胞术检测48例ITP患者及40名正常人外周血单个核细胞(PBMNC)表面共刺激分子CD80、CD86和CD137的表达;应用双抗体夹心酶联免疫吸附法(ELISA)检测血清PAIgG含量。结果表明:ITP患者CD80、CD86和CD137的表达水平分别为(4.92±2.02)%,(8.68±4.25)%,(5.32±2.67)%,PAIgG平均含量为210±3.02ng/107PA,均明显高于正常对照组(2.01±0.75)%,(4.56±2.06)%,(1.37±1.25)%和20±1.13ng/107PA(p<0.01)。共刺激分子表达水平与PAIgG含量呈正相关(r=0.302,p<0.05),与患者血小板数量呈负相关(r=-0.369,p<0.05)。结论:共刺激分子CD80、CD86和CD137是参与ITP发病和免疫反应的重要共刺激分子,其过度表达与ITP发病及临床病情密切相关。纠正其异常表达、调节免疫状态可能是ITP的治疗策略之一,具有重要的临床研究意义。

This study was aimed to detect the expression of co-stimulatory molecules CD80, CD86 and CD137 in peripheral blood of patients with idiopathic thrombocytopenic purpura （ ITP）, the content of platelet antibodies in serum （PAIgG）, and to analyze the relationship between them and their correlation with the number of platelet in peripheral blood, so as to clarify the roles of co-stimulatory molecules in pathogenesis of idiopathic thrombocytopenic purpura and evaluation of disease status. The co-stimulatory molecules CD80, CD86 and CD137 in peripheral blood mononuclear cells （PBMNCs） of 48 ITP patients and 40 normal persons were detected by immunofluorescence and flow cytometry （FACS）, PAIgG content in serum was detected by enzyme-linked immunosorbent assay （ELISA）. The results showed that CD80, CD86 and CD137 expression levels in ITP patients were （4.92 ± 2.02 ）%, （8.68 ± 4.25 ）%, （5.32 ± 2. 67 ） % respectively, PAIgG content was 210 ± 3.02 ng/107 PA, all these of which were significantly higher than these in normal control group （2.01 ±0.75） %, （4.56 ± 2.06） %, （ 1.37 ± 1.25 ） %, PAIgG 20 ± 1.13 ng/107 PA （p 〈 0. 01 ）. Correlation of co-stimulatory molecule expression with PAIgG content were positive （ r = 0. 302, p 〈 0.05 ）, but correlation of co-stimulatory molecule expression with platelet number was negative （ r = - 0. 369, p 〈 0.05 ）. It is concluded that the co-stimulatory molecules CD80, CD86 and CD137 are involved in immune response and the incidence of ITP. Their over-expression closely associates with the pathogenesis of ITP and clinical status, so that correcting the abnormal expression and regulating the immune status may be one therapeutic strategy and have important clinical significance.