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The regulation of erythropoiesis in man
1Department of Haematology, U.C.M.S.M., London.
The physiological role of erythropoietin (epo) as a "maintenance" and "progression" factor of terminal erythroid maturation is well established. The role of early acting erythroid factors in the maintenance of steady state erythropoiesis has not been ascertained. Primitive erythroid precursor cells (burst forming units) require a biological activity for colony formation in culture, which has been designated burst promoting activity (BPA) before it became clear that granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin 3 (IL-3) are (probably among others) important components of "BPA". Unlike epo, neither GM-CSF nor IL-3 have been detected in the circulation in sufficient amounts to allow recognition of feed back mechanisms between failing erythropoiesis and either of the two factors. Rather, GM-CSF and IL-3 may play a local role in the enhancement of erythropoiesis in the bone marrow, which is resistant to study in vivo. gamma-Interferon and transforming growth factor beta inhibit erythropoiesis in vitro. Their causative role in diseases with depressed erythropoiesis, however, is not proven.
The physiological role of erythropoietin (epo) as a "maintenance" and "progression" factor of terminal erythroid maturation is well established. The role of early acting erythroid factors in the maintenance of steady state erythropoiesis has not been ascertained. Primitive erythroid precursor cells (burst forming units) require a biological activity for colony formation in culture, which has been designated burst promoting activity (BPA) before it became clear that granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin 3 (IL-3) are (probably among others) important components of "BPA". Unlike epo, neither GM-CSF nor IL-3 have been detected in the circulation in sufficient amounts to allow recognition of feed back mechanisms between failing erythropoiesis and either of the two factors. Rather, GM-CSF and IL-3 may play a local role in the enhancement of erythropoiesis in the bone marrow, which is resistant to study in vivo. gamma-Interferon and transforming growth factor beta inhibit erythropoiesis in vitro. Their causative role in diseases with depressed erythropoiesis, however, is not proven.