Proliferation of Hemopoietic Colony-forming Cells Transplanted into Irradiated Mice.

It is generally agreed that survival of mice after whole-body irradiation depends on the restoration of hemopoietic function. This restoration may result from the proliferative activity of cells that have survived the radiation, or of cells from unirradiated donors that have been transplanted into the irradiated animals. Recently, we have suggested that such hemopoietic restoration depends in large measure on the activity of a class of cells that can be recognized by their ability to give rise to cellular colonies in the spleens of irradiated mice (1). The evidence relating colony-forming ability to survival of the animal is as follows: First, analysis of the cellular composition of colonies shows that they include both new colony-forming cells (2) and more differentiated erythrocytic, myelocytic, and megakaryocytic elements (3); thus colony-forming cells have the capacity for self-renewal which is necessary for continuing hemopoietic function, and the capacity to give rise to differentiated cells which are necessary for the survival of the animal. Second, the kinetics of repair of damage to colony-forming cells between fractionated doses of radiation is very similar to the kinetics of repair of radiation injury leading to death (1). This similarity supports the suggestion that an increase in the number of cells with colony-forming ability may form an important part of the cellular basis of repair of radiation damage where death is the criterion of injury. After sublethal irradiation, the restoration process in hemopoietic tissue may be considered to consist of two major phases, "early" and "late" repair (1). Early repair, which occurs during the first day after irradiation, is probably primarily the result of an intracellular process of recovery which takes place in sublethally damaged cells, in the absence of cellular proliferation. This recovery process has