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tvi
ka*
*
Division of Experimental Immunology and Immunopathology, Department of Pathology, and
Department of Microbiology and Immunology, University of Louisville, Louisville, KY 40292;
Department of Pathology, Brigham and Women’s Hospital, Boston, MA 02115; and
§
Center for Blood Research and Department of Pathology, Harvard Medical School, Boston, MA 02115.
ß-Glucans were identified 36 years ago as a biologic response
modifier that stimulated tumor rejection. In vitro studies have shown
that ß-glucans bind to a lectin domain within complement receptor
type 3 (CR3; known also as Mac-1, CD11b/CD18, or
Mß2-integrin, that functions as an
adhesion molecule and a receptor for factor I-cleaved C3b, i.e., iC3b)
resulting in the priming of this iC3b receptor for cytotoxicity of
iC3b-opsonized target cells. This investigation explored mechanisms of
tumor therapy with soluble ß-glucan in mice. Normal mouse sera were
shown to contain low levels of Abs reactive with syngeneic or
allogeneic tumor lines that activated complement, depositing C3 onto
tumors. Implanted tumors became coated with IgM, IgG, and C3, and the
absent C3 deposition on tumors in SCID mice was reconstituted with IgM
or IgG isolated from normal sera. Therapy of mice with glucan- or
mannan-rich soluble polysaccharides exhibiting high affinity for CR3
caused a 57–90% reduction in tumor weight. In young mice with lower
levels of tumor-reactive Abs, the effectiveness of ß-glucan was
enhanced by administration of a tumor-specific mAb, and in SCID mice,
an absent response to ß-glucan was reconstituted with normal IgM or
IgG. The requirement for C3 on tumors and CR3 on leukocytes was
highlighted by therapy failures in C3- or CR3-deficient mice. Thus, the
tumoricidal function of CR3-binding polysaccharides such as ß-glucan
in vivo is defined by natural and elicited Abs that direct iC3b
deposition onto neoplastic cells, making them targets for circulating
leukocytes bearing polysaccharide-primed CR3. Therapy fails when tumors
lack iC3b, but can be restored by tumor-specific Abs that deposit iC3b
onto the tumors.
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