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The immunotherapeutic potential of activated canine alveolar macrophages and antitumor monoclonal antibodies in metastatic canine melanoma.
|Title||The immunotherapeutic potential of activated canine alveolar macrophages and antitumor monoclonal antibodies in metastatic canine melanoma.|
|Publication Type||Journal Article|
|Year of Publication||1999|
|Authors||Soergel SA, MacEwen EG, Vail DM, Potter DM, Sondel PM, Helfand SC|
|Journal||Journal of immunotherapy (Hagerstown, Md. : 1997)|
|Date Published||1999 Sep|
|Keywords||Adjuvants, Immunologic, Animals, Antibodies, Monoclonal, Antigens, Neoplasm, Antineoplastic Agents, Cytotoxicity Tests, Immunologic, Dogs, Dose-Response Relationship, Immunologic, Immunotherapy, Active, Interferon-gamma, Recombinant, Lipopolysaccharides, Lung Neoplasms, Macrophage Activation, Macrophages, Alveolar, Melanoma, Tumor Cells, Cultured|
A variety of immune cell activators can enhance the cytotoxic effects of monocytes/macrophages including interferon-gamma (IFN-gamma) and muramyl peptides, which are under investigation for cancer therapy in humans and dogs. Pulmonary alveolar macrophages (PAMs) in particular, are strategically located within the lung and provide a potential defense against cancer cells metastatic to the lung. For this reason, we examined the in vitro cytotoxic potential of fresh and IFN-gamma-activated PAMs from normal dogs targeted to canine malignant melanoma cells with antiganglioside monoclonal antibodies (mAbs). Antiganglioside mAbs 14.G2a (anti-GD2) and R24 (anti-GD3), both in clinical trials for human neuroectodermal tumors including melanoma, significantly enhanced the cytotoxicity of canine melanoma mediated by canine PAMs. Further, the cytotoxicity mediated by recombinant canine IFN-gamma-activated canine PAMs, in combination with anti-GD2 ganglioside mAb 14.G2a, enhanced melanoma cytotoxicity above that seen with mAb 14.G2a alone. This documentation of antibody-dependent cellular cytotoxicity mediated by activated PAMs suggests that activation and targeting of resident pulmonary immune cells be pursued as a means to control pulmonary metastases.
|Alternate Journal||J. Immunother.|