GENETIC-CONTROL OF HLA-A AND B-ANTIGENS IN SOMATIC-CELL HYBRIDS - REQUIREMENT FOR BETA-2 MICROGLOBULIN
GENETIC-CONTROL OF HLA-A AND B-ANTIGENS IN SOMATIC-CELL HYBRIDS - REQUIREMENT FOR BETA-2 MICROGLOBULIN
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DOI：
10.1111/j.1399-0039.1978.tb01233.x
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发表时间：
1978-01-01
期刊：
影响因子：
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通讯作者：
BODMER, WF
中科院分区：
文献类型：
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作者：
ARCEGOMEZ, B;JONES, EA;BODMER, WF
[伯基特淋巴瘤]细胞系Daudi缺乏HLA-A和HL-A-B抗原和β 2微球蛋白。从该细胞系和[胸骨骨髓] D98/AH-2细胞之间的融合衍生的体细胞杂交体表达在任一亲本细胞上均检测不到的4种HLA抗原，即，A1、A10（Aw 26）、Bw 16（Bw 38）和Bw 17。通过吸收针对靶T [胸腺衍生的]淋巴细胞的反应，从而避免了由于污染抗Ia [免疫应答相关抗原]抗体引起的问题，并通过用鸡抗人β 2微球蛋白血清预处理阻断反应，证实了通过直接细胞毒性测定的初始定义。新的特异性是由于Daudi HLA区域，这一发现得到了证实，Daudi和A9 L之间的种间杂交，含有一条人类6号染色体，表达A10和Bw 17。这也将Daudi的单倍型定义为A10（Aw 26），Bw 17和A1，Bw 16（Bw 38）。Daudi HLA-A和HL-A-B抗原在2组独立杂交体中的再表达表明其在HLA区域中不携带突变。此前有报道称，与Daudi的体细胞杂种（包含15号染色体）不表达人β 2微球蛋白。Daudi上缺乏HLA-A和HL-A-B抗原的原因可能是由于β 2微球蛋白基因中的突变而产生的次级效应。
The [Burkitt''s lymphoma] cell line Daudi lacks HLA-A and HL-A-B antigens and .beta.2 microglobulin. Somatic cell hybrids derived from a fusion between this line and [sternal marrow] D98/AH-2 cells expressed 4 HLA antigens not detectable on either parent cell, i.e., A1, A10(Aw26), Bw16(Bw38) and Bw17. The initial definition by direct cytotoxicity assay was confirmed by absorption of reactions against target T [thymus-derived] lymphocytes, thus avoiding problems due to contaminating anti-Ia [immune response-associated antigen] antibodies, and by blocking the reactions by pretreatment with a chicken anti-human .beta.2 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 HL-A-B antigens in 2 independent sets of hybrids indicates that it does not carry a mutation in the HLA region. It was previously reported that somatic cell hybrids with Daudi, which contain chromosome 15, do not express human .beta.2 microglobulin. The reason for the lack of HLA-A and HL-A-B antigens on Daudi is probably a secondary effect due to the mutation(s) in the .beta.2 microglobulin gene.