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Sialoadhesin expression by bone marrow macrophages derived from Ehrlich-tumor-bearing mice.

Abstract
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.
AuthorsS Kusmartsev, J M Ruiz de Morales, J Rullas, M G Danilets, J L Subiza
JournalCancer immunology, immunotherapy : CII (Cancer Immunol Immunother) Vol. 48 Issue 9 Pg. 493-8 (Dec 1999) ISSN: 0340-7004 [Print] Germany
PMID10602886 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Culture Media, Conditioned
  • Membrane Glycoproteins
  • Neoplasm Proteins
  • Plastics
  • Receptors, Immunologic
  • Sialic Acid Binding Ig-like Lectin 1
  • Siglec1 protein, mouse
Topics
  • Animals
  • Bone Marrow Cells (metabolism, pathology)
  • Carcinoma, Ehrlich Tumor (blood)
  • Cell Adhesion
  • Cells, Cultured
  • Culture Media, Conditioned (pharmacology)
  • Disease Progression
  • Macrophages (metabolism, pathology)
  • Macrophages, Peritoneal (metabolism)
  • Membrane Glycoproteins (biosynthesis, genetics)
  • Mice
  • Mice, Inbred C57BL
  • Neoplasm Proteins (biosynthesis, genetics)
  • Plastics
  • Receptors, Immunologic (biosynthesis, genetics)
  • Rosette Formation
  • Sialic Acid Binding Ig-like Lectin 1

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