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Characterization of Tumor Binding by the IC-21 Macrophage Cell Line¹

Divisions of Pulmonary Medicine [E. K. C., E. M. S., J. D. H.] and Gastroenterology [P. S. L.], Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland 21201

The purpose of this study was to determine if the SV40-transformed murine macrophage cell line IC-21 is a suitable model to study the selective high avidity binding of tumor cells by subpopulations of activated macrophages. IC-21 macrophages bound P815, RBL5, and EL-4 murine tumor cells with high avidity, as measured by the inverted centrifugation method. Tumor binding by IC-21 macrophages was competitively inhibited by crude membrane vesicles prepared from tumor cells but not by cell membranes prepared from nontransformed splenic leukocytes, suggesting that this process was mediated by tumor-specific binding sites. IC-21 macrophages and primary cultures of pyran copolymer-elicited peritoneal macrophages demonstrated similar tumor binding avidity, kinetics, saturability, and metabolic requirements for optimal high avidity tumor binding. However, compared with primary cultures of pyran copolymer-elicited peritoneal macrophages, IC-21 macrophages bound 4-fold more tumor cells and were more homogeneous for tumor binding capability. Finally, one third of maximal tumor cell binding by IC-21 macrophages was completed within 5 min of contact with tumor, suggesting that IC-21 macrophages constituitively expressed some high avidity tumor binding sites. Their stable and homogeneous capability for binding tumor cells and their ease of growth make the IC-21 macrophage cell line a potentially valuable model for elucidating the molecular mechanisms responsible for selective high avidity tumor binding by subpopulations of activated macrophages.

¹ This work was supported by Veterans Administration Merit Review Grant 128444284-0002 and grants from the American Lung Association of Maryland, the Maryland Cancer Program/American Cancer Society Institutional Grant IN-147F (University of Maryland), and the University of Maryland Medical Biotechnology Center.

² Supported by the Work-Study Program of the University of Maryland Baltimore County and a Short Term Research Training grant from the University of Maryland School of Medicine.

³ Supported by NIH Grant RO1 A1 21844 and V. A. Merit Review.

⁴ Supported by Veterans Administration Research Associate Award 128444284-0003. To whom requests for reprints should be addressed, at University of Maryland at Baltimore, 10 South Pine Street, MSTF Bldg., Rm. 800, Baltimore, MD 21201.

Received 6/21/89. Revised 4/ 9/90.