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Altered erythrocytes and a leaky block in B-cell development in
CD24/HSA-deficient mice
PJ Nielsen, B Lorenz, AM Muller, RH Wenger, F Brombacher, M Simon, T von der Weid, WJ Langhorne, H Mossmann and G Kohler
Max Planck Institute for Immunobiology, Freiburg, Germany.
The heat stable antigen (HSA, or murine CD24) is a glycosyl
phosphatidylinositol-linked surface glycoprotein expressed on immature
cells of most, if not all, major hematopoietic lineages, as well as in
developing neural and epithelial cells. It has been widely used to stage
the maturation of B and T lymphocytes because it is strongly induced and
then repressed again during their maturation. Terminally differentiated
lymphocytes, as well as most myeloid lineages, are negative for HSA.
Erythrocytes are an exception in that they maintain high levels of HSA
expression. HSA on naive B cells has been shown to mediate cell-cell
adhesion, while HSA on antigen-presenting cells has been shown to mediate a
costimulatory signal important for activating T lymphocytes during an
immune response. Here, we characterize mice that lack a functional HSA
gene, constructed by homologous recombination in embryonic stem cells.
While T-cell and myeloid development appears normal, these mice show a
leaky block in B-cell development with a reduction in late pre-B and
immature B-cell populations in the bone marrow. Nevertheless, peripheral
B-cell numbers are normal and no impairment of immune function could be
detected in these mice in a variety of immunization and infection models.
We also observed that erythrocytes are altered in HSA-deficient mice. They
show a higher, tendency to aggregate and are more susceptible to hypotonic
lysis in vitro. In vivo, the mean half-life of HSA-deficient erythrocytes
was reduced. When infected with the malarial parasite Plasmodium chabaudi
chabaudi, the levels of parasite-bearing erythrocytes in HSA-deficient mice
were also significantly elevated, but the mice were able to clear the
infection with kinetics similar to wild-type mice and were immune to a
second challenge. Thus, apart from alterations in erythrocytes and a mild
block in B-cell development, the regulated expression of HSA appears to be
dispensable for the maturation and functioning of those cell lineages that
normally express it.
Volume 89,
Issue 3,
pp. 1058-1067,
02/01/1997
Copyright © 1997 by The American Society of Hematology
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