Tumor bound immunoglobulins: The relationship between the in vivo coating of tumor cells by potentially cytotoxic anti-tumor antibodies, and the expression of immune complex receptors

✍ Scribed by Gary Braslawsky; Maya Ran; Isaac P. Witz

• Publisher: John Wiley and Sons
• Year: 1976
• Tongue: French
• Weight: 497 KB
• Volume: 18
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.2910180115

✦ Synopsis

Abstract

In this study we investigated the relationship between binding of anti‐tumor antibodies by polyoma‐virus‐induced SEYF‐a tumor cells and the expression of immune‐complex receptors on these cells. It was shown that in vivo propagated cells became progressively coated with IgG. The increase in the IgG coating of SEYF‐a cells, occurring during the second week of propagation, was directly correlated with an increase in the coating of cells with potentially cytotoxic anti‐tumor antibodies. The activity of these antibodies was demonstrated by cell lysis following addition of exogenous complement. Cell populations propagated in vivo for longer periods (3 weeks or more) became less sensitive to exogenous complement although their IgG coating remained high, and although higher titers of anti‐tumor antibodies could be eluted from them. This indicated that antibodies coating young tumor cell populations have the capacity to activate complement whereas those coating older tumor cell populations are incapable of complement activation. Previous findings that SEYF‐a cell populations are able to bind unrelated immune complexes were confirmed in the present study. We also found that the capacity of these populations to bind such unrelated complexes decreased with propagation time in vivo. The involvement of anti‐tumor antibodies in this phenomenon was indicated by the finding that such antibodies inhibited binding of unrelated immune complexes by young cells but not by old cells. Furthermore, treatments causing dissociation of Ig from the cell surface restored, to some extent, the capacity of anti‐tumor antibodies to inhibit immune complex binding by old SEYF‐a populations.