Lonai P, Rechavi G, Arman E, Givol D
EMBO J. 1983;2(5):781-6. doi: 10.1002/j.1460-2075.1983.tb01500.x.
Retention or loss of immunoglobulin heavy chain genes was studied in 20 functional T cell hybridoma clones. DNA probes representing C mu, C alpha and JH genes, as well as VH subgroups II and III were hybridized with restriction enzyme fragments of hybridoma DNA by the Southern filter hybridization technique. Parental alleles of the hybridoma cells were distinguished on the basis of polymorphism of the lengths of restriction enzyme fragments. All clones retained the alleles of the lymphoma parent cell BW-5147 at all four loci. Thirteen clones lost both CH and VH alleles of the immune partner cell, whereas seven retained both VH alleles, and at least C alpha of the antigen-specific partner. Hence, T cell function in these cells is compatible with the loss of most immunoglobulin heavy chain alleles. This is interpreted to indicate either gene rearrangement and deletion, or chromosome loss. Accordingly, the T cell receptor is either controlled by two split gene loci in chromosome 12, at the two respective (5' and 3') ends of the mouse heavy chain gene family, or by a gene(s) outside chromosome 12.
在20个功能性T细胞杂交瘤克隆中研究了免疫球蛋白重链基因的保留或缺失情况。通过Southern印迹杂交技术，将代表Cμ、Cα和JH基因以及VH亚组II和III的DNA探针与杂交瘤DNA的限制性酶切片段进行杂交。根据限制性酶切片段长度的多态性来区分杂交瘤细胞的亲本等位基因。所有克隆在所有四个位点均保留了淋巴瘤亲本细胞BW-5147的等位基因。13个克隆丢失了免疫伙伴细胞的CH和VH等位基因，而7个克隆保留了VH等位基因以及抗原特异性伙伴细胞的至少Cα基因。因此，这些细胞中的T细胞功能与大多数免疫球蛋白重链等位基因的缺失是相容的。这被解释为表明基因重排和缺失，或染色体丢失。相应地，T细胞受体要么由位于小鼠重链基因家族两个各自（5'和3'）末端的12号染色体上的两个分裂基因座控制，要么由12号染色体以外的一个基因控制。
