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Prepublished online as a Blood First Edition Paper on August 15, 2002; DOI 10.1182/blood-2002-01-0096.
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Blood, 15 December 2002, Vol. 100, No. 13, pp. 4427-4432
HEMATOPOIESIS
Fas-mediated apoptosis is important in regulating cell
replication and death in trisomy 8 hematopoietic cells but not in cells
with other cytogenetic abnormalities
Elaine M. Sloand,
Sonnie Kim,
Monika Fuhrer,
Antonio M. Risitano,
Ryotaro Nakamura,
Jaroslaw P. Maciejewski,
A. John Barrett, and
Neal S. Young
From the Hematology Branch, National Heart, Lung, and
Blood Institute, Bethesda, MD.
Increased apoptosis of hematopoietic progenitor cells has
been implicated in the pathophysiology of cytopenias associated with
myelodysplastic syndromes (MDSs), and inhibition by immunosuppression may account for the success of this treatment in some patients. We
examined bone marrow and peripheral blood of 25 patients with chromosomal abnormalities associated with MDS (monosomy 7, trisomy 8, and 5q ) for evidence of apoptosis. When fresh bone marrow was
examined, the number of apoptotic and Fas-expressing CD34 cells was
increased in patients with trisomy 8, but decreased in monosomy 7, as
compared with healthy control donor marrow. Fas expression was
increased in the trisomy 8 cells and decreased in the monosomy 7 cells
when compared with normal cells from the same patient. Trisomy 8 cells
were more likely to express activated caspase-3 than were normal cells.
For bone marrow cells cultured with Fas agonist or Fas antagonist, the
percentage of cells with trisomy 8 was significantly decreased in most
cases after Fas receptor triggering and increased by Fas ligand (Fas-L)
antagonist (P < 0.01), suggesting increased Fas
susceptibility of cells with trisomy 8. No such changes were seen in
cultures of cells with 5q or monosomy 7. Fas antagonist facilitated
the expansion of cells with trisomy 8 only. Cells with trisomy 8 appear
to be more susceptible to Fas-mediated apoptosis. Clinical data
demonstrating the responsiveness of some patients with trisomy 8 to
anti-thymocyte globulin (ATG) and cyclosporine (CsA) would favor an
active role of the immune system in this syndrome.
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