Faanes R B, Choi Y S, Good R A
J Exp Med. 1973 Jan 1;137(1):171-82. doi: 10.1084/jem.137.1.171.
Isoantiserum (IS) inhibition of lymphocyte-mediated cytotoxicity (LMC) was studied using an in vitro (51)Cr release assay system. In the early phase of incubation, LMC was competitively inhibited by IS. However, as the incubation continued, LMC irreversibly overcame IS inhibition (the "escape" phenomenon). Addition of fresh antiserum did not alter the course of the escape. Low-temperature incubation of isoantibody-coated target cells delayed the onset of the escape. We have excluded the possibility that the escape phenomenon is induced by complement or by LMC mediated by antigen-antibody complex. It is hypothesized that antibody directed toward an actively metabolizing target cell induces an alteration in the cell membrane that alters further interaction with the antibody. However, sensitivity to lymphocyte cytotoxicity is maintained.
使用体外(51)铬释放测定系统研究了同种抗血清(IS)对淋巴细胞介导的细胞毒性(LMC)的抑制作用。在孵育早期,LMC受到IS的竞争性抑制。然而,随着孵育的继续,LMC不可逆地克服了IS的抑制作用(“逃逸”现象)。添加新鲜抗血清并未改变逃逸的进程。对包被有同种抗体的靶细胞进行低温孵育可延迟逃逸的发生。我们排除了逃逸现象是由补体或抗原-抗体复合物介导的LMC所诱导的可能性。据推测,针对活跃代谢的靶细胞的抗体可诱导细胞膜发生改变,从而改变与抗体的进一步相互作用。然而,对淋巴细胞细胞毒性的敏感性得以维持。