DEFECT OF ERYTHROPOIESIS IN NON-LEUKAEMIC AKR MICE

Publisher Website
Google Scholar
Abstract
The kinetics of the CFU [colony forming units] population and erythropoiesis were investigated in the AKR strain mouse prior to the onset of thymic leukemias. Hemopoiesis was compared in syngeneic AKR, semi-allogenic C3H and (C3H .times. AKR) F1 mice injected with AKR stem cells. The reduction in the number of spleen colonies previously described by Perkins, et al. in syngeneic hosts, as compared to semi-allogenic C3H hosts, was actually related to defective erythropoiesis resulting from a dysfunction of the AKR hemopoietic inductive microenvironment (HIM). Erythropoietin secretion was normal in AKR mice. The early hemopoietic events were related to the stem cell. Lodgement of the CFU (''f'' factor) and doubling time were not disturbed, but the onset of CFU proliferation was markedly delayed in the AKR strain. The main expression of the AKR HIM dysfunction was a significant reduction in the number of erythroid (E) colonies and an impaired output of red blood cells per E colony in the syngeneic host as compared to the allogenic one. A weakly histoincompatible system, such as that in C3H and hybrid hosts, did not interfere with the stages of hemopoiesis except by lengthening the doubling time of the CFU. The prevalent influence of HIM was emphasized.
Keywords