Howell D N, Kostyu D D, Ting J P, Cresswell P
Somat Cell Mol Genet. 1984 May;10(3):217-24. doi: 10.1007/BF01535244.
Expression of class I histocompatibility antigens (HLA-A and B) on hybrids of human T and B lymphoblastoid cell lines (LCL) was examined. The T-LCL CEM expressed low levels of HLA-A and B antigens. CEMR and CEMR .3, two 8-azaguanine- and ouabain-resistant sublines of CEM used for fusion, expressed no detectable HLA-B antigens and expressed HLA-A antigens at a level below that of CEM. The three B-LCL studied expressed class I histocompatibility antigens at levels 50- to 80-fold in excess of that found on CEM as assessed by indirect immunofluorescence and flow cytometry. Total levels of class I histocompatibility antigens on hybrids of CEMR and CEMR .3 with B-LCL were similar to those found on the B-LCL. CEM-encoded HLA-A and B antigens were expressed on the hybrids at levels much greater than those seen on CEM itself; expression by the hybrids of CEM-encoded and B-LCL-encoded class I antigens was comparable. By RNA-DNA filter hybridization, CEMR .3 was found to have extremely low levels of class I heavy-chain mRNA compared with two B-LCL and with HSB, a T-LCL that expresses high levels of class I histocompatibility antigens. Thus, the paucity of HLA-A and B expression by CEMR .3 (and by inference, CEMR and CEM), as well as the enhancement of CEM-encoded HLA-A and B antigen expression on B-LCL X T-LCL hybrids, must be due, at least in part, to modulation of the level of transcripts encoding HLA class I heavy chains.
对人T和B淋巴母细胞系（LCL）杂交体上I类组织相容性抗原（HLA - A和B）的表达进行了检测。T - LCL CEM表达低水平的HLA - A和B抗原。用于融合的CEM的两个对8 - 氮杂鸟嘌呤和哇巴因耐药的亚系CEMR和CEMR.3，未检测到HLA - B抗原表达，且HLA - A抗原表达水平低于CEM。通过间接免疫荧光和流式细胞术评估，所研究的三个B - LCL表达的I类组织相容性抗原水平比CEM上的高出50至80倍。CEMR和CEMR.3与B - LCL杂交体上I类组织相容性抗原的总水平与B - LCL上的相似。CEM编码的HLA - A和B抗原在杂交体上的表达水平远高于CEM自身；CEM编码的和B - LCL编码的I类抗原在杂交体上的表达相当。通过RNA - DNA滤膜杂交发现，与两个B - LCL以及表达高水平I类组织相容性抗原的T - LCL HSB相比，CEMR.3的I类重链mRNA水平极低。因此，CEMR.3（以及由此推断的CEMR和CEM）HLA - A和B表达的缺乏，以及B - LCL×T - LCL杂交体上CEM编码的HLA - A和B抗原表达的增强，至少部分原因必定是编码HLA I类重链的转录本水平受到了调控。
