Descamps-Latscha B, Feuillet-Fieux M N, Baruchel A, Patereau C, Nguyen A T
C R Acad Sci III. 1984;298(15):419-22.
We have previously shown that monoclonal anti-T cell antibodies bound to their specific targets can trigger the activation of monocyte/macrophage oxidative metabolism through an Fc receptor-mediated interaction. The present study demonstrates that IgG coated platelets from patients with thrombocytopenia-associated diseases can induce a similar respiratory burst activation in polymorphonuclear and mononuclear phagocytes from normal individuals. The intensity of the oxidative reaction as measured by luminol-dependent chemiluminescence is in close correlation with the level of surface-bound IgG molecules as determined by a radioactive anti-immunoglobulin assay. This new methodology to evaluating IgG fixed on human platelets by their capacity to trigger the generation of highly reactive oxygen species by granulocytes and monocytes has also suggested a new mechanism in the genesis of thrombocytopenia associated with autoimmune diseases.
我们之前已经表明，与特定靶点结合的单克隆抗T细胞抗体可通过Fc受体介导的相互作用触发单核细胞/巨噬细胞氧化代谢的激活。本研究表明，血小板减少相关疾病患者的IgG包被血小板可在正常个体的多形核和单核吞噬细胞中诱导类似的呼吸爆发激活。通过鲁米诺依赖性化学发光测量的氧化反应强度与通过放射性抗免疫球蛋白测定法确定的表面结合IgG分子水平密切相关。这种通过粒细胞和单核细胞触发高活性氧生成的能力来评估人血小板上固定的IgG的新方法，也提示了自身免疫性疾病相关血小板减少发生的新机制。
