The Lyb-2 phenotype of hemolytic PFC.
The Lyb-2 phenotype of hemolytic PFC.
复制标题
溶血性 PFC 的 Lyb-2 表型。
DOI：
10.1007/bf01572594
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发表时间：
1980
期刊：
影响因子：
3.2
通讯作者：
Tang,L
中科院分区：
文献类型：
--
作者：
Yakura,H;Shen,FW;Boyse,EA;Tang,L
同种异体抗原的Lyb-2系统（Sato和Boyse 1976）由4号染色体上的g基因座决定（Sato等1977，Taylor和Shen 1977），其具有三个等位基因，抗原Lyb-2.1、-2.2和-2.3各一个，推测的第四个等位基因仅由小鼠品系STS/A代表，其不表达迄今鉴定的三种Lyb-2同种抗原中的任何一种Lyb-2的表达局限于B细胞谱系这一点没有争议，但关于Lyb-2在溶血性空斑形成细胞（PFC）上表达的证据是相互矛盾的。BALB浆细胞瘤中Lyb-2.2的缺失表明PFC的Lyb-2表型为阴性，但有几个已发表和未发表的观察结果表明，Lyb-2抗血清和补体的细胞溶解消除了PFC，尽管部分和不一致。我们希望通过使用同源小鼠作为PFC供体来解决这个问题，但是使用Lyb-2.1抗血清和补体的免疫细胞溶解消除试验的结果被混淆，因为同源（B6-Lyb-2.1）和伴侣（B6）小鼠品系的PFC减少，无疑是由于污染抗体，该污染抗体在细胞毒性试验中既没有定义也没有太多证据。幸运的是，现在通过使用单克隆Lyb-2.1抗体解决了这个问题，该抗体明确表明PFC是Lyb-2，B6小鼠（Lyb-2.2）和B6-Lyb-2.1同类小鼠（N= 8;等位基因供体I/St）是从Sloan-Kettering研究所的菌落中获得的。为了生产单克隆Lyb-2.1抗体，根据K6 hler和Milstein（1975），将来自用DBA/2脾细胞（Lyb-2.1）免疫的BALB/c小鼠（Lyb-2.2）的脾细胞与P3/NSI/1-Ag 4 -1融合，产生产生抗Lyb-2.1抗体的克隆（9-6.1）。通过菌株分布确定Lyb-2.1的特异性，包括B6（Lyb-2.2）与通过常规Lyb-2.1抗血清分型获得的同源B6-Lyb-2.1菌株的关键区别。吸收分析表明仅限于B细胞，也与常规LyB-2.1抗血清的结果一致（Sato and Boyse 1976）。单克隆抗Lyb-2.1（来自降植烷致敏的BALB/c小鼠的腹水，携带9-6.1
The Lyb-2 system of alloantigens (Sato and Boyse 1976) is determined by g locus on chromosome 4 (Sato et al. 1977, Taylor and Shen 1977) which has three alleles, one each for antigens Lyb-2.1,-2.2, and-2.3, and a presumed fourth allele represented solely by mouse strain STS/A which expresses none of the three Lyb-2 alloantigens so far identified (Shen et al. 1977).There has been no dispute that expression of Lyb-2 is confined to the B-cell lineage, but the evidence concerning expression of Lyb-2 on hemolytic plaqueforming cells (PFC) is conflicting. Absence of Lyb-2.2 from BALB plasmacytomas suggests that the Lyb-2 phenotype of PFC is negative, yet there are several published and unpublished observations that cytolysis with Lyb-2 antiserum and complement eliminates PFC, albeit partially and inconsistently. We hoped to resolve this problem by using congenic mice as donors of PFC, but results of immune-cytolytic elimination tests with Lyb-2.1 antiserum and complement were confused because of reduction of PFC both from the congenic (B6-Lyb-2.1) and from the partner (B6) mouse strains, doubtless by contaminant antibody that has been neither defined nor much in evidence in cytotoxicity assays. Fortunately the question has now been settled by use of a monoclonal Lyb-2.1 antibody which indicates decisively that PFC are Lyb-2, B6 mice (Lyb-2.2) and B6-Lyb-2.1 congenic mice (N= 8; allele donor I/St) were obtained from colonies maintained at Sloan-Kettering Institute. For the production of monoclonal Lyb-2.1 antibody, spleen cells from BALB/c mice (Lyb-2.2) immunized with DBA/2 spleen cells (Lyb-2.1) were fused with P3/NSI/1-Ag4-1 according to K6hler and Milstein (1975), yielding a clone (9-6.1) producing antibody against Lyb-2.1. Specificity for Lyb-2.1 was established by strain distribution, including the critical distinction of B6 (Lyb-2.2) from the congenic B6-Lyb-2.1 strain which was derived by typing with conventional Lyb-2.1 antiserum. Absorption analysis, indicative of restriction to B cells, also conformed to findings with conventional Lyb-2.1 antiserum (Sato and Boyse 1976). The titer of monoclonal anti-Lyb-2.1 (from ascites of pristane-primed BALB/c mice bearing 9-6.1