Moulds J M, Arnett F C, Giles C G, Hamilton R G
Division of Rheumatology and Clinical Immunogenetics, University of Texas Health Science Center, Houston.
Complement Inflamm. 1990;7(2):95-101. doi: 10.1159/000463134.
Utilizing mouse monoclonal antibodies which recognize Rodgers 1 and Chido 1 epitopes carried on the C4A and C4B molecules, and heat-aggregated IgG to activate C1, an immunoassay was developed for the quantitation of total C4 as well as C4A and C4B. Interassay variation was 12.4, 11.5 and 10.8%, respectively. The immunoassay was compared to the quantitation of total C4 by radial immunodiffusion by testing 103 random white controls and gave a Pearson's product-moment correlation coefficient of 0.81. Three genetic total-C4-deficient individuals were nonreactive in all three assays. This activated assay is specific, reproducible, and superior to existing methods for the quantitation of C4A and C4B and detection of the heterozygous C4 null state.
利用识别C4A和C4B分子上携带的Rodgers 1和Chido 1表位的小鼠单克隆抗体，以及热聚集的IgG来激活C1，开发了一种免疫测定法用于定量总C4以及C4A和C4B。批间变异分别为12.4%、11.5%和10.8%。通过检测103个随机白人对照，将该免疫测定法与通过放射免疫扩散法定量总C4进行比较，得到的Pearson积矩相关系数为0.81。三名遗传性总C4缺陷个体在所有三种测定中均无反应。这种激活测定法具有特异性、可重复性，并且优于现有的定量C4A和C4B以及检测杂合C4无效状态的方法。
