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Gamma-interferon modulates human monocyte/macrophage transferrin receptor
expression
R Taetle and JM Honeysett
Department of Pathology, U.C.S.D. Cancer Center.
Although circulating human monocytes do not express transferrin (Tf)
receptors, cultured adherent blood cells display high-affinity Tf binding
sites. In the present studies, effects of various cytokines and
biologically active proteins on human monocyte/macrophage Tf receptors were
investigated. After culture, Tf receptor expression by adherent blood cells
was time dependent and plateaued by 7 days. The addition of interleukin-1
(IL-1), alpha-interferon (alpha-IFN), granulocyte/macrophage-colony
stimulating factor (GM-CSF), or human IgG to macrophages cultured for 4
days did not alter Tf receptor expression. Fe-saturated, human Tf caused a
significant, dose-dependent decrease in receptor expression. At a dose of
100 U/mL, gamma- interferon (gamma-IFN) significantly increased Tf receptor
expression by macrophages cultured for 4 (230% +/- 51% of control) or 7
days (150% +/- 22%). Scatchard analyses showed increased binding sites but
no change in receptor affinity. Northern and slot blot analysis of cellular
mRNA from macrophages cultured for 4 to 7 days and exposed to gamma-IFN
showed a two- to fivefold increase in Tf receptor mRNA, but less than or
equal to 30% increase in beta-actin mRNA. Ferritin content of
gamma-IFN-treated macrophages was 47% to 63% of control cells. Net uptake
of 59Fe from Tf by gamma-IFN-treated cells was 10% to 17% of control, but
uptake of radiolabeled Tf was comparable. When macrophages were labeled
with 59Fe and then exposed to gamma-IFN, cell-associated Fe was reduced by
43%, indicating that gamma-IFN caused macrophage Fe release. gamma-IFN
specifically modulates Tf receptor display by inducing Fe release and
reducing cellular Fe content. Regulation of Tf receptor expression in
macrophages is controlled by cellular Fe content and is thus similar to
regulatory mechanisms in dividing cells.
Volume 71,
Issue 6,
pp. 1590-1595,
06/01/1988
Copyright © 1988 by The American Society of Hematology
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