Experimental and clinical investigations on stem cell take and colony formation.
First, lymphocyte transplantation into total body-irradiated rats is discussed. The effect on spleen colony formation caused by the transplantation of untreated lymphocytes, as well as of lymphocytes previously incubated with PHA, or with PHA plus L-asparaginase, or with lymphokines, was studied. Then the effect of the urinary colony-stimulating factor in vitro, and the in vitro feeder-layer activity of leucocytes on colony formation of human and mice bone marrow cells in haematological diseases is dealth with. The injection of rat lymphocytes previously incubated for 24 hours with PHA resulted in a higher number and a larger size of colonies in the spleen of the recipient rats. Lymphocytes preincubated with lymphokines gave rise to the formation of spleen colonies which were larger than those developing after the injection of untreated lymphocytes. When the lymphocytes were previously incubated with PHA plus L-asparaginase, PHA failed to stimulate colony formation in the spleen. The phenomenon is explained by assuming that PHA, as an aspecific stimulator of cell division, initiated the division of CFUs, thus the CFUs content of the preincubated samples increased, resulting in an increase in the number of colonies formed after the transplantation of lymphocytes pretreated with PHA. Another possible explanation is that CFUs division, or their spleen take is enhanced by the immunocompetent lymphocytes activated by PHA, either directly or via soluble mediators produced or released by immunocompetent lymphocytes such as lymphokines. The study of colony-forming cells and colony-stimulating activity in primary myelofibrosis (PM) showed an increase in the number of circulating CFUc in this condition, and an abnormal density of these cells reaching a peak below 1.062. The lowering of CSA in the first two peripheral blood gradient fractions agrees with the observation in the same fractions of a high percentage of CFUc at the expense of the CSC population. Thus, double cell population seems to exist in PM. One is greatly abnormal with a low specific density and high plating efficiency, whereas the other population is almost normal, showing a higher specific density and a lower plating efficiency.
Experimental and clinical investigations on stem cell take and colony formation. First, lymphocyte transplantation into total body-irradiated rats is discussed. The effect on spleen colony formation caused by the transplantation of untreated lymphocytes, as well as of lymphocytes previously incubated with PHA, or with PHA plus L-asparaginase, or with lymphokines, was studied. Then the effect of the urinary colony-stimulating factor in vitro, and the in vitro feeder-layer activity of leucocytes on colony formation of human and mice bone marrow cells in haematological diseases is dealth with. The injection of rat lymphocytes previously incubated for 24 hours with PHA resulted in a higher number and a larger size of colonies in the spleen of the recipient rats. Lymphocytes preincubated with lymphokines gave rise to the formation of spleen colonies which were larger than those developing after the injection of untreated lymphocytes. When the lymphocytes were previously incubated with PHA plus L-asparaginase, PHA failed to stimulate colony formation in the spleen. The phenomenon is explained by assuming that PHA, as an aspecific stimulator of cell division, initiated the division of CFUs, thus the CFUs content of the preincubated samples increased, resulting in an increase in the number of colonies formed after the transplantation of lymphocytes pretreated with PHA. Another possible explanation is that CFUs division, or their spleen take is enhanced by the immunocompetent lymphocytes activated by PHA, either directly or via soluble mediators produced or released by immunocompetent lymphocytes such as lymphokines. The study of colony-forming cells and colony-stimulating activity in primary myelofibrosis (PM) showed an increase in the number of circulating CFUc in this condition, and an abnormal density of these cells reaching a peak below 1.062. The lowering of CSA in the first two peripheral blood gradient fractions agrees with the observation in the same fractions of a high percentage of CFUc at the expense of the CSC population. Thus, double cell population seems to exist in PM. One is greatly abnormal with a low specific density and high plating efficiency, whereas the other population is almost normal, showing a higher specific density and a lower plating efficiency.