Smith M D, Verroust P J, Adam C, Galceran M, Morel-Maroger L
Clin Exp Immunol. 1977 Dec;30(3):364-9.
Significant levels of EAC-rosette inhibition compared to control subjects were found in the sera of patients with focal and segmental hyalinosis (FSH), membranoproliferative glomerulonephritis (MPGN) and extra-membranous glomerulonephritis (EGN). In patients with IgA disease, although some sera produced high levels of inhibition, the group as a whole did not differ significantly from the controls. Evidence was obtained suggesting that the rosette inhibitory activity was due to immune complexes (IC) bearing C3 rather than C3 fragments. Firstly, the inhibitory activity was precipitable by 4% PEG, a concentration which does not precipitate the C3 fragments. Secondly, the inhibitory activity was selectively removed from the PEG precipitates by an anti-human immunoglobulin G immunoabsorbent. Finally, since it had been suggested that in some instances an unknown serum factor could inhibit EAC-rosette formation and activation of the alternative pathway of complement, the latter was studied and found to be normal in all the sera studied. Taken together, these results suggest that the inhibition of EAC-rosette formation obtained with the sera of the patients studied was due to the presence in these sera of some material behaving as IC. No clear-cut association was, however, seen between rosette inhibition and the presence or absence of Ig or C3 deposits in the kidney.
在局灶节段性玻璃样变(FSH)、膜增生性肾小球肾炎(MPGN)和膜性肾小球肾炎(EGN)患者的血清中,发现与对照受试者相比,EAC玫瑰花结抑制水平显著升高。在IgA肾病患者中,尽管一些血清产生了高水平的抑制作用,但作为一个整体,该组与对照组没有显著差异。有证据表明,玫瑰花结抑制活性是由于带有C3的免疫复合物(IC)而非C3片段所致。首先,抑制活性可被4%的聚乙二醇(PEG)沉淀,该浓度不会沉淀C3片段。其次,通过抗人免疫球蛋白G免疫吸附剂可从PEG沉淀物中选择性去除抑制活性。最后,由于有人提出在某些情况下,一种未知的血清因子可抑制EAC玫瑰花结形成和补体替代途径的激活,因此对后者进行了研究,发现所有研究的血清中其均正常。综上所述,这些结果表明,所研究患者血清对EAC玫瑰花结形成的抑制作用是由于这些血清中存在一些表现为IC的物质。然而,在玫瑰花结抑制与肾脏中Ig或C3沉积的有无之间未发现明确的关联。