Peritoneal ceils of anemic donors enriched with macrophages at the expense of Tcell lysis using anti-Thy-1.2 monoclonal antibodies are capable of triggering various routes of terminal erythroid differentiation characteristic of stress erythropoiesis during their adoptive transfer to normal syngeneic recipients. Stimulation of the proliferation of polychromatophilic erythroblasts and initiation of mitoses in oxyphilic erythroblasts are regulated by interacting T ceUs and macrophages, and the "reserve erythropoiesis" mainly by macrophages.
Key Words: stress erythropoiesis; peritoneal cells; reserve erythropoiesis; blood lossIn mammals with severe anemias the erythroid precursors, on reaching the terminal stages, form red ceils as a result of terminal differentiation by various routes. One of these routes, "reserve erythropoiesis," is an emergency route of accelerated differentiation of ceils providing for the survival of the organism during the early periods after massive blood loss. It consists in the omission of severn terminal stages and the rapid release of morphologically immature cells into the blood [2,3,[6][7][8]. A transito13" increase in the content of basophilic erythroblasts (BE) in the bone marrow paralleled by a decrease of their mitotic activity may be considered as a bone marrow marker of "reserve erythropoiesis" [3,7]. Moreover, blood loss enhances polychromatophilic erythroblasts (PE) amplification and initiates mitoses in oxyphilic erythroblasts (OE), which normally almost never divide [1,3].
Thirty minutes after massive blood loss, peritoneal cells gained the ability to trigger reparative erythropoiesis in the bone marrow of normal syngeneic recipients. This was manifested in proliferation of oxyphilic erythroblasts and activation of the reserve pathway of erythroid differentiation 4 days after cell transplantation. The maximum transfer capacity of peritoneal cells was observed 4 h after blood loss, but 4 days later they only initiated mitoses in oxyphilic erythroblasts.
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