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Hyaluronate-CD44 interactions can induce murine B-cell activation
A Rafi, M Nagarkatti and PS Nagarkatti
Department of Biology, Virginia-Maryland Regional College of Veterinary
Medicine, Virginia Polytechnic Institute and State University, Blacksburg
24061, USA.
CD44 is a widely distributed cell surface glycoprotein whose principal
ligand has been identified as hyaluronic acid (HA), a major component of
the extracellular matrix (ECM). Recent studies have demonstrated that
activation through CD44 leads to induction of effector function in T cells
and macrophages. In the current study, we investigated whether HA or
monoclonal antibodies (MoAbs) against CD44 would induce a proliferative
response in mouse lymphocytes. Spleen cells from normal and nude, but not
severe combined immunodeficient mice, exhibited strong proliferative
responsiveness to stimulation with soluble HA or anti-CD44 MoAbs.
Furthermore, purified B cells, but not T cells, were found to respond to
HA. HA was unable to stimulate T cells even in the presence of antigen
presenting cells (APC) and was unable to act as a costimulus in the
presence of mitogenic or submitogenic concentrations of anti-CD3 MoAbs. In
contrast, stimulation of B cells with HA in vitro, led to B-cell
differentiation as measured by production of IgM antibodies in addition to
increased expression of CD44 and decreased levels of CD45R. The fact that
the B cells were responding directly to HA through its binding to CD44 and
not to any contaminants or endotoxins was demonstrated by the fact that
F(ab)2 fragments of anti- CD44 MoAbs or soluble CD44 fusion proteins could
significantly inhibit the HA-induced proliferation of B cells. Also,
HA-induced proliferation of B cells was not affected by the addition of
polymixin B, and B cells from lipopolysaccharide (LPS)-unresponsive C3H/HeJ
strain responded strongly to stimulation with HA. Furthermore, HA, but not
chondroitin- sulfate, another major component of the ECM, induced B-cell
activation. It was also noted that injection of HA intraperitoneally,
triggered splenic B cell proliferation in vivo. Together, the current study
demonstrates that interaction between HA and CD44 can regulate murine B-
cell effector functions and that such interactions may play a critical role
during normal or autoimmune responsiveness of B cells.
Volume 89,
Issue 8,
pp. 2901-2908,
04/15/1997
Copyright © 1997 by The American Society of Hematology
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