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Inhibition of murine erythroid colony formation in vitro by interferon
gamma and correction by interferon receptor immunoadhesin
RT Means , SB Krantz, J Luna, SA Marsters and A Ashkenazi
Hematology Division, Vanderbilt University School of Medicine, Nashville,
TN.
It has been previously reported that inhibition of human erythroid
colony-forming units (CFU-E) in vitro by interleukin-1 (IL-1) is an
indirect effect, occurring through the production of interferon gamma (IFN
gamma). IFN gamma, in turn, inhibits CFU-E colony formation directly, and
its inhibitory effect can be overcome by exposure to high concentrations of
erythropoietin (EPO). To develop an in vitro animal model for investigating
inhibition of erythropoiesis by IFN gamma, the effects of recombinant
murine (rm) IFN gamma on highly purified CFU-E from the spleens of mice
infected with the anemia strain of the Friend virus (FVA) were studied.
rmIFN gamma inhibited CFU-E colony formation in a dose-dependent manner.
This inhibition occurred with large (> or = 8 cell) colonies only;
smaller colonies were not affected. The inhibitory effect was corrected to
72% of control by high EPO concentrations of 64 U/mL. Murine CFU-E were
then cultured with rmIFN gamma in the presence of a soluble murine IFN
gamma receptor fused to the hinge and Fc domains of the human IgG1 heavy
chain (mIFN gamma R- IgG). Inhibition of CFU-E colony formation by rmIFN
gamma (100 U/mL) was corrected by mIFN gamma R-IgG in a dose-dependent
manner, with an approximate IC50 of 0.05 nmol/L, and complete or near
complete correction at 0.5 nmol/L. Similarly, a human IFN gamma R-IgG
greatly reduced the inhibitory effect of recombinant human IFN gamma on
human CFU-E. These experiments provide an in vitro animal model for
studying the inhibitory effects of IFN gamma on erythropoiesis and indicate
that IFN gamma R-IgG may be a useful agent for reducing the toxicity of IFN
gamma in vivo.
Volume 83,
Issue 4,
pp. 911-915,
02/15/1994
Copyright © 1994 by The American Society of Hematology
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