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Inhibition of human erythroid colony-forming units by gamma interferon can
be corrected by recombinant human erythropoietin [see comments]
RT Means and SB Krantz
Department of Medicine, Department of Veterans Affairs Medical Center,
Nashville, TN 37212.
Tumor necrosis factor (TNF), interleukin-1 (IL-1), and gamma interferon
(gamma IFN) inhibit erythropoiesis in vivo and in vitro, and have been
implicated in the pathogenesis of the anemia of chronic disease. Anemia in
patients with rheumatoid arthritis and in animals exposed chronically to
IL-1 and TNF can be corrected by the administration of recombinant
erythropoietin (Epo). We exposed highly purified human erythroid
colony-forming units (CFU-E) cultured from peripheral blood burst-forming
units-erythroid (BFU-E) and unpurified human marrow CFU-E to recombinant
human gamma IFN and showed inhibition of colony formation in vitro. This
inhibition was reversed by increased concentrations of Epo. The mechanisms
by which this effect occurs are unknown at present. Epo may cause a
downregulation of gamma IFN receptor expression on CFU-E or, alternatively,
gamma IFN may cause a downregulation of Epo receptor expression. A full
understanding of these mechanisms awaits a more complete comprehension of
the regulation of erythropoiesis; however, the effect of Epo in vitro is
similar to its ability to correct the anemia of chronic disease in vivo.
Volume 78,
Issue 10,
pp. 2564-2567,
11/15/1991
Copyright © 1991 by The American Society of Hematology
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