Sialoadhesin (sheep erythrocyte receptor, SER) is a macrophage-restricted adhesion molecule that binds certain sialylated
ligands. It is borne by bone marrow stromal macrophages, promoting the interaction with developing myeloid cells, and by a subset of tissue macrophages involved in antigen presentation and activation of
tumor-reactive T cells. The expression of
sialoadhesin on SER+ macrophages is not constitutive but requires the continuous supply of a
sialoadhesin-inducing serum factor.
Tumor growth is often associated with marked alterations of myelopoiesis and impairment of T cell activation; yet the expression of
sialoadhesin in macrophages derived from
tumor bearers has not been addressed. The aim of this study was to assess whether Ehrlich
tumor (ET) - a murine mammary
carcinoma - growth may modify the
sialoadhesin expression by bone marrow macrophages and/or
sialoadhesin-inducing activity in ET-bearing sera. Moreover, putative functional
sialoadhesin inhibitors produced by ET cells were tested. The results indicate that bone marrow cells from ET bearers show a seven- to eight-fold decrease in SER+ cells as detected by flow cytometry. This is accompanied by an overall decrease in sheep erythrocyte binding to
tumor-bearer-derived bone marrow cells, but also by lower numbers of
plastic-adherent cells. Functional
sialoadhesin expression is preserved at the single-cell level and no inhibitors are found in ET-bearing sera or ET cell culture supernatants.
Tumor progression does not impair the
sialoadhesin-inducing activity of ET-bearing sera, or the ability of SER- macrophages (e.g. peritoneal macrophages) to respond to such an induction. In conclusion, while SER+ macrophages are greatly decreased in bone marrow from ET bearers, this is not due to a down-regulation of
sialoadhesin expression, nor to an impairment of
sialoadhesin-inducing factor or to the presence of
sialoadhesin-binding moieties of
tumor origin, but, more likely, to a decrease of fully mature macrophages.