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体细胞杂种中 HLA - A 和 B 抗原的遗传控制:对β2微球蛋白的需求。

The genetic control of HLA-A and B antigens in somatic cell hybrids: requirement for beta2 microglobulin.

作者信息

Arce-Gomez B, Jones E A, Barnstable C J, Solomon E, Bodmer W F

出版信息

Tissue Antigens. 1978 Feb;11(2):96-112. doi: 10.1111/j.1399-0039.1978.tb01233.x.

Abstract

The lymphoblastoid cell line Daudi lacks both HLA-A and B antigens and beta2 microglobulin. Somatic cell hybrids derived from a fusion between this line and D98/AH--2 were shown to express four HLA antigens not detectable on either parent cell, A1, A10(Aw26), Bw16(Bw38, Bw17. The initial definition by direct cytotoxicity assay was confirmed by absorption of reactions against target T lymphocytes, thus avoiding problems due to contaminating Ia antibodies, and by blocking the reactions by pretreatment with a chicken anti-human beta2 microglobulin serum. That the new specificities were due to the Daudi HLA region was confirmed by the finding that interspecific hybrids between Daudi and A9L, containing a single human chromosome 6, expressed A10 and Bw17. This also defined the haplotypes of Daudi as A10(Aw26), Bw17 and A1, Bw16(Bw38). The re-expression of the Daudi HLA-A and B antigens in two independent sets of hybrids indicates that it does not carry a mutation in the HLA region. It has previously been reported that somatic cell hybrids with Daudi, which contain chromosome 15, do not express human beta2 microglobulin. These results suggest that the reason for the lack of HLA-A and B antigens on Daudi is a secondary effect due to the mutation(s) in the beta2 microglobulin gene.

摘要

淋巴母细胞系Daudi既缺乏HLA - A和B抗原,也缺乏β2微球蛋白。由该细胞系与D98/AH - 2融合产生的体细胞杂种显示表达四种在任何一个亲代细胞上都检测不到的HLA抗原,即A1、A10(Aw26)、Bw16(Bw38、Bw17)。通过对针对靶T淋巴细胞的反应进行吸收,从而避免因Ia抗体污染而产生的问题,并通过用鸡抗人β2微球蛋白血清预处理来阻断反应,证实了直接细胞毒性试验的初始定义。发现Daudi与A9L(含有一条人类6号染色体)之间的种间杂种表达A10和Bw17,这证实了新的特异性是由于Daudi的HLA区域所致。这也确定了Daudi的单倍型为A10(Aw26)、Bw17和A1、Bw16(Bw38)。Daudi的HLA - A和B抗原在两组独立的杂种中重新表达,这表明它在HLA区域没有携带突变。此前有报道称,含有15号染色体的与Daudi的体细胞杂种不表达人β2微球蛋白。这些结果表明,Daudi缺乏HLA - A和B抗原的原因是β2微球蛋白基因突变的继发效应。

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