Manger B J, Krapf F E, Gramatzki M, Nüsslein H G, Burmester G R, Krauledat P B, Kalden J R
Scand J Immunol. 1985 Apr;21(4):369-73. doi: 10.1111/j.1365-3083.1985.tb01443.x.
In five patients with vasculitis, hypereosinophilia, and elevated serum IgE levels a diagnosis of Churg-Strauss syndrome was established. To identify a possible role of IgE in pathogenic mechanisms leading to the vasculitis, we performed a sequential precipitation of the patients' sera with different concentrations of polyethylene glycol (PEG) 6000. Using a radio immunosorbent test, we tested the precipitates obtained for IgE. Considerable amounts of IgE were traced in the serum precipitates of all patients, especially after the second precipitation step (4.0% PEG). In contrast, no IgE-containing precipitates were detectable in sera from patients with different allergic diseases and high IgE serum levels. Together with an increase in C3d serum levels and the failure to demonstrate C1q-binding material in patients' sera, these data suggest the involvement of IgE-containing immune complexes in the pathogenesis of Churg-Strauss vasculitis, activating the complement via the alternate pathway.
在5例患有血管炎、嗜酸性粒细胞增多和血清IgE水平升高的患者中,确诊为变应性肉芽肿性血管炎。为了确定IgE在导致血管炎的致病机制中可能发挥的作用,我们用不同浓度的聚乙二醇(PEG)6000对患者血清进行连续沉淀。使用放射免疫吸附试验,我们检测了所获得沉淀中的IgE。在所有患者的血清沉淀中均检测到大量IgE,尤其是在第二个沉淀步骤(4.0% PEG)之后。相比之下,在患有不同过敏性疾病且血清IgE水平高的患者血清中未检测到含IgE的沉淀。这些数据连同患者血清中C3d水平的升高以及未能证明C1q结合物质,提示含IgE的免疫复合物参与变应性肉芽肿性血管炎的发病机制,通过替代途径激活补体。