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Blood, Vol. 94 No. 8 (October 15), 1999:
pp. 2613-2621
Increased Fetal and Extramedullary Hematopoiesis in Fas-Deficient
C57BL/6-lpr/lpr Mice
Elke Schneider,
Géraldine Moreau,
Anne Arnould,
Florence Vasseur,
Naushad Khodabaccus,
Michel Dy, and
Sophie Ezine
From the Université René Descartes-Paris V, CNRS UMR
8603, Paris, France; INSERM U345, Paris, France; and Institut Necker,
Paris, France.
In this study, we examined the consequences of Fas deficiency on
hematopoiesis in C57BL/6-lpr/lpr mice. We found a striking extramedullary increase in hematopoietic progenitor cells, comprising erythroid and nonerythroid lineages alike. These modifications preceded
the lymphadenopathy, because early progenitors (colony-forming units-spleen [CFU-S] day 8) were already augmented in
day-18 fetal livers of the lpr phenotype. Three weeks after
birth, CFU-S increased in peripheral blood and spleen and
colony-forming cells (CFU-C) began to accumulate 1 to 3 weeks later.
Extramedullary myelopoiesis augmented progressively in Fas-deficient
mice, reaching a maximum within 6 months. By then, mature and immature
myeloid cells had infiltrated the spleen, the liver, and the peritoneal
cavity. Similar changes occurred in C57BL/6-gld/gld mice,
indicating that they resulted from Fas/FasL interactions. Medullary
hematopoiesis was not significantly modified in adult mice of either
strain. Yet, the incidence of CFU-S decreased after Fas cross-linking on normal bone marrow cells in the presence of interferon  ,
consistent with a regulatory function of Fas/FasL interactions in early
progenitor cell development. These data provide evidence that Fas
deficiency can affect hematopoiesis both during adult and fetal life
and that these modifications occur independently from other pathologies associated with the lpr phenotype.
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