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Antibody-Dependent Cytotoxicity: Modulation by the Cytochalasins and Microtubule-Disruptive Agents¹

From the Department of Immunology, Research Institute, The Hospital For Sick Children, Toronto, Canada and the Max-Planck-Institute für Immunobiologie, Freiburg, Germany

Abstract

Cytochalasin B was shown to inhibit lysis of antibodycoated target cells by effector cells from rabbit spleen and lymph node. The inhibitory activity was dose-dependent and reversible. At low concentrations of cytochalasin B (0.15 to 0.3 µg/ml) enhancement of antibody-dependent cytotoxicity was observed. The drug appeared to act at an early stage of the lytic pathway after effector cell-target cell interaction, but before triggering of the cytotoxic event. Cytochalasin A was shown to be a more potent but similarly reversible inhibitor of antibody-dependent cytotoxicity. No enhancement of cytotoxicity was seen at non-inhibitory concentrations of cytochalasin A. The microtubule-disruptive agents colchicine (10^-4 M), vinblastine (10^-5 M) and colcemid (10^-6 M) did not influence antibody-dependent cytotoxicity at concentrations which were not toxic to the effector cells. Our results suggest that antibody-dependent cytotoxicity is a surface membrane-initiated process and microtubule-associated functions are not essential.

Footnotes

¹ This work was supported by Grant MA 4875 from the Medical Research Council of Canada and a grant from the Deutsche Forschungsgemeinschaft.

² Correspondence should be addressed to Dr. E. W. Gelfand, Department of Immunology, The Hospital For Sick Children, 555 University Avenue, Toronto, Canada M5G 1X8.

³ Present address: Institute for Immunology, Heidelberg, Germany.