Guldner H H, Netter H J, Szostecki C, Lakomek H J, Will H
Max Planck Institut für Biochemie, Martinsried, Federal Republic of Germany.
J Immunol. 1988 Jul 15;141(2):469-75.
Several cDNA fragments encoding parts of the (U1)RNP specific 68-kDa autoantigen were expressed in Escherichia coli and the fusion proteins were used as substrate for localization of the autoreactive epitopes. We have identified a region of approximately 30 amino acids reacting with more than 90% (16 of 17) of all human anti-p68 sera tested, regions which carry only a few and a region with no autoepitopes. Comparative analysis of epitopes recognized on partially degraded fusion proteins indicated that the anti-p68 autoimmune response is polyclonal. It involves generation of antibodies to several epitopes including one in a region with retroviral gag protein homology speculated to play a role in the initiation of the autoimmune response. Each of the 17 sera tested contained a different set of autoantibody specificities. These data are not consistent with random mutation as a sole mechanism of anti-p68 autoantibody induction and argue for an Ag-driven autoimmune response.
编码（U1）RNP特异性68 kDa自身抗原部分片段的几个cDNA片段在大肠杆菌中表达，这些融合蛋白被用作自身反应性表位定位的底物。我们已经鉴定出一个约30个氨基酸的区域，它能与所检测的所有人类抗p68血清中超过90%（17份中的16份）发生反应，还有一些携带少量自身表位的区域以及一个没有自身表位的区域。对部分降解的融合蛋白上识别的表位进行比较分析表明，抗p68自身免疫反应是多克隆的。它涉及针对几个表位产生抗体，其中一个表位位于与逆转录病毒gag蛋白具有同源性的区域，推测该区域在自身免疫反应的起始中起作用。所检测的17份血清中的每一份都含有不同的自身抗体特异性组合。这些数据与随机突变作为抗p68自身抗体诱导的唯一机制不一致，支持抗原驱动的自身免疫反应。
