Weissbarth E, Baruth B, Mielke H, Liman W, Deicher H
Rheumatol Int. 1982;2(2):67-73. doi: 10.1007/BF00541248.
Sera from patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) were assessed for in vitro platelet activation as measured by serotonin release; 24% (30) of 124 tested RA sera and 51% (35) of 69 SLE sera induced a significant 3H serotonin release. Investigation of 17 synovial fluid samples from RA patients revealed significant release in 82%. Concomitant testing for lymphocytotoxic antibodies and immune complexes did not show any correlation to platelet activation. Upon gel filtration the release-inducing activity of positive sera was localized in the region of 160 000 Daltons. Further characterization by ion exchange chromatography, immune electrophoresis, chromatographic and SDS PAGE molecular weight determinations, as well as analytical ultracentrifugation all confirmed the IgG nature of the release-inducing protein. Negative blocking experiments performed by preincubation of platelets with Fc-IgG fragments prior to challenge with a release-inducing serum excluded the participation of Fc receptors in the reaction. It was concluded that the release was caused by a platelet reactive IgG antibody. This antibody may also cause release of platelet mediators in vivo and may thus contribute to the pathogenesis of the generalized vasculopathy in both diseases.
对类风湿性关节炎(RA)和系统性红斑狼疮(SLE)患者的血清进行了体外血小板活化评估,通过血清素释放进行测定;在124份检测的RA血清中,24%(30份)以及在69份SLE血清中,51%(35份)诱导了显著的3H血清素释放。对17份RA患者的滑液样本进行研究发现,82%出现显著释放。同时检测淋巴细胞毒性抗体和免疫复合物,未显示与血小板活化有任何相关性。经凝胶过滤后,阳性血清的释放诱导活性定位于160000道尔顿区域。通过离子交换色谱、免疫电泳、色谱法和SDS - PAGE分子量测定以及分析超速离心进行的进一步表征均证实了释放诱导蛋白的IgG性质。在用释放诱导血清攻击之前,通过用Fc - IgG片段预孵育血小板进行的阴性阻断实验排除了Fc受体参与该反应。得出的结论是,释放是由血小板反应性IgG抗体引起的。这种抗体也可能在体内导致血小板介质的释放,因此可能促成这两种疾病中全身性血管病变的发病机制。