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Fas antigen expression on CD34+ human marrow cells is induced by interferon
gamma and tumor necrosis factor alpha and potentiates cytokine-mediated
hematopoietic suppression in vitro
J Maciejewski, C Selleri, S Anderson and NS Young
Hematology Branch, National Heart, Lung, and Blood Institute, National
Institutes of Health, Bethesda, MD 20892, USA.
Activation of Fas antigen, a cell surface receptor molecule, by its ligand
results in transduction of a signal for cell death. The Fas system has been
implicated in target cell recognition, clonal development of immune
effector cells, and termination of the cellular immune response. Fas
antigen expression on lymphocytes is regulated by interferon gamma (IFN
gamma) and tumor necrosis factor alpha (TNF alpha), cytokines that also
have inhibitory effects on hematopoiesis. We investigated Fas antigen
expression on human marrow cells and the effects of Fas activation on
hematopoiesis in vitro. Freshly isolated immature hematopoietic cells, as
defined by the CD34 marker, did not express Fas antigen at levels
detectable by fluorescent staining. CD34+ cells, which include progenitors
and stem cells, showed low levels of Fas expression in culture, even in the
presence of growth factors. Stimulation by TNF alpha and IFN gamma markedly
increased Fas antigen expression on CD34+ cells. Anti-Fas antibody, which
mimics the action of the putative ligand, enhanced IFN gamma- and TNF
alpha-mediated suppression of colony formation by bone marrow (BM) in a
dose-dependent manner. This effect did not require the presence of
accessory cells. Colony formation from mature (CD34+ CD38+) and immature
(CD34+ CD38-) progenitor cells and long-term culture initiating cells were
susceptible to the inhibitory action of anti-Fas antibody in the presence
of IFN gamma and TNF alpha. Apoptosis assays performed on total BM cells
and CD34+ cells showed that anti-Fas antibody induced programmed cell death
of CD34+ BM cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Volume 85,
Issue 11,
pp. 3183-3190,
06/01/1995
Copyright © 1995 by The American Society of Hematology
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