Surface Remodelling of Reticulocytes produced in Response to Erythroid Stress

Abstract

ACCELERATED erythropoiesis is associated with the production of reticulocytes of excessive size, perhaps as the result of skipped divisions during erythroid cell proliferation in the bone marrow¹. Isotopic studies have been interpreted as showing that these “stress reticulocytes” are short-lived and are replaced by progressively smaller cells with more normal life spans^1–6. It has recently been suggested, however, that stress reticulocytes are not destroyed in toto but are made smaller by a process of remodelling or surface fragmentation⁷; loss of only portions of these cells could explain most of the isotopic findings, although the residual cells might remain intact.