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Blood, Vol. 93 No. 3 (February 1), 1999:
pp. 796-803
Apoptotic Role of Fas/Fas Ligand System in the Regulation of
Erythropoiesis
R. De Maria,
U. Testa,
L. Luchetti,
A. Zeuner,
G. Stassi,
E. Pelosi,
R. Riccioni,
N. Felli,
P. Samoggia, and
C. Peschle
From the Department of Hematology-Oncology, Istituto Superiore di
Sanita', Rome, Italy; the Kimmel Cancer Center, Thomas Jefferson
University, Philadelphia, PA; and the Department of Surgical,
Anatomical and Oncological Sciences, Institute of Human Anatomy,
University of Palermo, Palermo.
The possible involvement of Fas and Fas ligand (FasL) in the
regulation of erythropoiesis was evaluated. Immunohistochemistry of
normal bone marrow specimens revealed that several immature erythroblasts undergo apoptosis in vivo. Analysis of bone marrow erythroblasts and purified progenitors undergoing unilineage erythroid differentiation showed that Fas is rapidly upregulated in early erythroblasts and expressed at high levels through terminal maturation. However, Fas crosslinking was effective only in less mature
erythroblasts, particularly at basophilic level, where it induced
apoptosis antagonized by high levels of erythropoietin (Epo). In
contrast, FasL was selectively induced in late differentiating
Fas-insensitive erythroblasts, mostly at the orthochromatic stage. FasL
is functional in mature erythroblasts, as it was able to kill
Fas-sensitive lymphoblast targets in a Fas-dependent manner.
Importantly, FasL-bearing mature erythroblasts displayed a Fas-based
cytotoxicity against immature erythroblasts, which was abrogated by
high levels of Epo. These findings suggest the existence of a negative
regulatory feedback between mature and immature erythroid cells,
whereby the former cell population might exert a cytotoxic effect on
the latter one in the erythroblastic island. Hypothetically, this
negative feedback operates at low Epo levels to moderate the
erythropoietic rate; however, it is gradually inhibited at increasing
Epo concentrations coupled with enhanced erythrocyte production. Thus,
the interaction of Fas and FasL may represent an apoptotic control
mechanism for erythropoiesis, contributing to the regulation of red
blood cell homeostasis.
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