Different reactivity of rat alveolar and peritoneal macrophages with EAMC and anti-CR3 monoclonal antibodies.

Resident alveolar macrophages of murine species are known to bind complement-coated bacteria and erythrocytes (EAMC, EAMC3b and EAMiC3b) significantly less well than do resident peritoneal macrophages. Because of the potential importance of C3 receptors of resident alveolar macrophages in pulmonary host defenses, we studied the expression of iC3b (CR3) receptors on rat resident alveolar and peritoneal macrophages with a sensitive cytofluorometric method, employing mouse anti-human CR3 monoclonal antibodies. One monoclonal to CR3, designated M42, labelled rat alveolar macrophages as well as it labelled human alveolar macrophages (40.6% versus 45.3%, respectively), whereas rat peritoneal macrophages labelled significantly less well (13.6%-17.4%) (P less than 0.05). A second antihuman CR3 monoclonal, M44, labelled low, but essentially identical percentages of rat alveolar and peritoneal macrophages (21.2% and 23.3%, respectively). Binding of M42 and M44 to rat macrophages appeared to be specific for the CR3 receptor based on cytofluorometric analysis and on the fact that the monoclonals could inhibit the attachment of EAMC to rat macrophages. We conclude that there is specific binding of mouse anti-human CR3 anti-bodies to conserved epitopes of receptors on rat macrophages, and that CR3 expression on resident rat alveolar macrophages is greater than is indicated by attachment of complement-coated particles.