DEFICIENT GROWTH OF C57BL MARROW CELLS TRANSPLANTED IN F1 HYBRID MICE. ASSOCIATION WITH THE HISTOCOMPATIBILITY-2 LOCUS.
DEFICIENT GROWTH OF C57BL MARROW CELLS TRANSPLANTED IN F1 HYBRID MICE. ASSOCIATION WITH THE HISTOCOMPATIBILITY-2 LOCUS.
复制标题
F1 杂交小鼠中移植的 C57BL 骨髓细胞生长不足。
作者：
G. Cudkowicz;J. Stimpfling
用脾克隆技术和[~(131)I]~(131)I-5-脱氧尿嘧啶核苷测定受体小鼠脾中新生成的DNA，研究了C57BL、C3H和A系骨髓细胞移植到受照等基因、F1杂交和回交后代小鼠体内的增殖能力。与同基因和异基因宿主相比，C57BL细胞在(A×C57BL)F1和(C57BL×C3H)F1及正反交中生长不良，而C3H和A系骨髓移植在同基因、F1和回交受体中生长成功。在分离回交后代中，即在与C57BL雄性杂交的F1雌性后代中，C57BL嫁接的成功或失败的频率表明，该性状是由常染色体上的一对遗传决定因素控制的。后者显然与IXth连接基团中的H-2区域相连或部分连锁。实验证据还表明，在H-2杂合子中，C57BL造血细胞移植的失败与供体细胞因受体同种抗原过多而耗尽无关，而是与组织相容性相关生长要求尚未确定的杂合子中缺乏表达有关。这些要求对造血细胞是特定的，但对皮肤移植物不是，最可能是由于涉及H-2或H-2连锁基因的遗传(等位基因间)相互作用的影响。
The ability of C57BL, C3H, and A strain marrow cells to proliferate on transplantation into irradiated isogenic, F1 hybrid, and backcross progeny mice has been investigated by the spleen-colony technique and by measuring the newly-formed DNA in the recipient spleen with [131I] 5-iododeoxyuridine. Transplants of C57BL cells grew poorly in (A×C57BL)F1 and in (C57BL×C3H)F1 and reciprocal hybrids, as compared with isogenic and allogeneic hosts, whereas C3H and A strain marrow grafts were successful in isogenic, F1 hybrid and backcross recipients. In segregating backcross progeny, i.e. in offspring from F1 hybrid females mated to C57BL males, the frequency of success or failure of the C57BL grafts suggested that the trait was controlled by a single pair of genetic determinants at an autosomal locus. The latter is apparently linked with, or part of, the H-2 region in the IXth linkage group. The experimental evidence suggested also that the failure of C57BL haemopoietic cell grafts in H-2 heterozygotes was not related to exhaustion of donor cells by excess of recipient isoantigen but rather to lack of expression in the heterozygotes of histocompatibility-related growth requirements yet undefined. These requirements are specific for haemopoietic cells, but not for skin grafts, and resulted most probably from the effect of genetic (inter-allelic) interaction involving H-2 or an H-2-linked locus.