Zelený V, Lengerová A, Matousek V
Folia Biol (Praha). 1975;21(5):299-308.
Previous experiments showed that in the spleen of non-syngeneic (H-2 disparate) irradiated hosts, the colony-forming performance of injected bone marrow cells may be markedly lower than the standard syngeneic performance. There were also some indications that the deficit was due to a deviated differentiation of the pluripotent stem cells into an alternative pathway. In the present study, the total proliferative activity of donor bone marrow cells [B10.A(2R)] in the syngeneic or allogeneic [B10.A(5R)] hosts was measured as the rate of uptake of 125IUdR and the erythropoietic activity as the rate of uptake of 59Fe. Since both activities are linear functions of the number of injected cells, their inhibition in allogeneic hosts could be judged by the relative slopes of the comparable regression lines. Well reproducible results showed that the erythropoietic activity was inhibited more than the total proliferative activity; this suggests that the residual component of the total proliferative activity must be inhibited less (or even stimulated) in the allogeneic host. The possibility that the differential effect of the allogeneic host environment on the total and erythropoietic activities might be due to a deviated differentiation of some pluripotent cells into the lymphopoietic pathway is discussed.
先前的实验表明,在非同基因(H-2不匹配)受辐照宿主的脾脏中,注入的骨髓细胞的集落形成能力可能明显低于标准的同基因表现。也有一些迹象表明,这种缺陷是由于多能干细胞向另一条途径的分化偏离所致。在本研究中,测量了同基因或异基因[B10.A(5R)]宿主中供体骨髓细胞[B10.A(2R)]的总增殖活性,以125IUdR的摄取率表示,红细胞生成活性以59Fe的摄取率表示。由于这两种活性都是注入细胞数量的线性函数,因此它们在异基因宿主中的抑制作用可以通过可比回归线的相对斜率来判断。可重复的良好结果表明,红细胞生成活性的抑制比总增殖活性更明显;这表明在异基因宿主中,总增殖活性的残留成分受到的抑制一定较少(甚至受到刺激)。讨论了异基因宿主环境对总活性和红细胞生成活性的差异作用可能是由于一些多能细胞向淋巴细胞生成途径的分化偏离所致的可能性。