Binding of components of the properdin system to cultured human lymphoblastoid cells and B lymphocytes.

Abstract

A receptor for fluid phase human complement (C) components C3 and C3b (1, 2) was found on the surface membranes of human lymphoblastoid cells. No other C proteins or serum factors were needed to mediate binding of C3 or C3b to this receptor. In studying its biological importance, we demonstrated that Raji cells cultured in medium containing fresh normal human serum (NHS) 1 and cobra venom factor (CoF) were lysed (1). Results were similar when C3b-bearing Raji cells were cultured in medium with fresh NHS. In other experiments, lysis was eliminated by inactivating serum factor B. 2 Therefore, we concluded that C3b bound to the Raji cells activated the C system through C3b-dependent C3 convertase (3, 4) which resulted in fixation of the later C components directly on the cell membranes, thereby leading to their damage and lysis.Joseph et al. (5) observed that immune human serum, containing antimeasles virus antibody and C, lysed HeLa cells infected with measles virus via activation of the alternative C pathway (6). By using immunofluorescence, properdin (P) was detected on the surfaces of the measles virus-infected HeLa cells previously incubated with the immune serum (Perrin, L., and M. B. A. Oldstone, unpublished observations). Therefore we questioned, do components of the P system bind to cells, and if so, what events lead to their fixation on the cell surface? We now show that P, as well as factor B, can bind to surfaces of certain lymphoblastoid cells and of human B type peripheral lymphocytes. The fixation *

Complement-dependent cellular cytotoxicity: lymphoblastoid lines that activate complement component 3 (C3) and express C3 receptors have increased sensitivity to lymphocyte-mediated lysis in the presence of fresh human serum.

“…Interestingly, these results correlated with the expression of C3 receptors when detected with the monoclonal antibody reagents. The property of C3 activation by cells was attributed by Theofilopoulos to the presence of C3 receptors on their plasma membranes (27). Our results would lead to a similar conclusion.…”

Complement-Dependent Control of Teratoma Formation by Embryonic Stem Cells

“…We found (as have others) that given in sufficient numbers, embryonic stem cells can form tumors in mice with an intact complement system. Similar observations have been made for lymphoblastoid tumor cells (33)(34)(35). These cells are sensitive to complement in vitro but form tumors when introduced in vivo.…”

Evidence for the presence of receptors for c3 and IgG Fc on human synovial cells

“…Furthermore, since Gram negative bacteria activate the alternative complement pathway whereas IgM antibody-sensitized sheep red blood cells activate the classic complement pathway, the former indicator particles may carry, apart from the C3 fragments, additional complement components not present on EAC. These components may stabilize the C3 fragments (24) or play a role in the interaction of bacteria with synovial lining cells. It is also of importance to note that Traycoff et a1 (8) found that in contrast to a large percentage (> 80%) of sudanophilic cells that were considered to represent monocytes and monocyte-derived macrophages, a very small proportion (3%) of cells considered to be true lining cells derived from collagenase digested fresh human synovial membranes did form rosettes with EAC.…”