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An Anti-ICAM-2 (CD102) Monoclonal Antibody Induces Immune-mediated Regressions of Transplanted ICAM-2-negative Colon Carcinomas¹

Gene Therapy Unit, Department of Medicine, University of Navarra School of Medicine, 31008 Pamplona [I. M., I. G., G. M., V. S., M. R-C., I. T., J. P.]; Proteomics Facility and Department of Immunology and Oncology, Centro Nacional de Biotecnología (Pharmacia/ Consejo Superior de Investigaciones Cientificas), Canto Blanco, E-28049 Madrid [E. C., J. P. A.]; and Centro de Investigaciones Biológicas, Consejo Superior de Investigaciones Cientificas, 28006 Madrid [A. L. C., M. R.] Spain

Monoclonal antibodies (mAbs) can mediate antitumor effects by indirect mechanisms involving antiangiogenesis and up-regulation of the cellular immune response rather than by direct tumor cell destruction. From mAbs raised by immunization of rats with transformed murine endothelial cells, a mAb (EOL4G8) was selected for its ability to eradicate a fraction of established colon carcinomas that did not express the EOL4G8-recognized antigen. The antigen was found to be ICAM-2 (CD102). Antitumor effects of EOL4G8, which required a functional T-cell compartment, were abrogated by depletion of CD8⁺ cells and correlated with antitumor CTL activity, whereas only a mild inhibition of angiogenesis was observed. Interestingly, we found that EOL4G8 acting on endothelial ICAM-2 markedly enhances leukotactic factor activity-1-independent adhesion of immature dendritic cells to endothelium—an effect that is at least in part mediated by DC-SIGN (CD209).

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