Abstract
Chemical stimulation with endotoxin, estradiol or glucan has been used in conjunction with irradiation to modify various dynamic aspects of the RE system. Specific liver and spleen irradiation has been found to be as effective as whole body irradiation in suppressing the normal increase in RES activity and cell proliferation in the oestradiol stimulated mice. In contrast, irradiated animals were found to continue to respond to endotoxin stimulation. It has been concluded, therefore, that endotoxin stimulates largely by activation of existing cells while oestradiol stimulates largely by cell proliferation. Though these phagocytic cells in the liver may have had ancestral precursors from the bone marrow, we conclude from cell proliferation studies in stimulated animals that cell division of existing littoral cells is the predominant source of the increased number of hepatic macrophages.
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Selected References
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