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Augmentation of Lymphokine-activated Killer Cell Cytotoxicity by Monoclonal Antibodies against Human Small Cell Lung Carcinoma¹

Cancer Immunology Research Unit, Charles A. Sammons Cancer Center, Baylor University Medical Center, Dallas, Texas 75246

This study examined the lymphokine-activated killer (LAK) cell cytotoxicity on monoclonal antibody (MoAb)-bound tumor cells from the human small cell lung carcinoma cell lines H69 and H128. LAK cells were generated from normal peripheral blood mononuclear cells by incubation with interleukin 2 for 3 or more days. Cells from the LAK culture were cytotoxic to natural killer-sensitive (K562, 84% cytotoxicity) and natural killer-resistant (Daudi, 85%; H69 and H128, 69% and 97%, respectively) cell lines, and to freshly excised human lung (49%) and breast (57%) tumors. LAK cytotoxicity to H69 or H128 cells was significantly augmented by target cell preincubation with the small cell lung carcinoma-reactive MoAbs 1096 (increases of up to 271%) or 5023 (up to 223%). SCLC 5023 or 1096 did not enhance LAK cytotoxicity to Daudi cells of lymphoblastoid origin. Pretreatment of LAK cells with an anti-Fc receptor antibody blocked MoAb augmentation by 1096 or 5023 (but not LAK cytotoxicity), suggesting that LAK-MoAb interaction may be mediated by Fc binding. LAK activity coincided with emergence of a large cell [interleukin 2-stimulated large mononuclear leukocyte (LML)] subset expressing the CD16 and NKH-1 surface determinants. Serial immunophenotyping of the LAK cell culture harvested at Days 3, 5, and 7 indicated that the level of LAK cytotoxicity, with or without MoAb augmentation, correlated with frequency of NKH-1-reactive LMLs. These observations support the hypothesis that LAK cytotoxicity is mediated by a NKH-1-reactive LML subpopulation. Antitumor cytotoxicity may be augmented by tumor-reactive MoAbs through Fc binding to this LML subset.

¹ Supported in part by grants from the Barbara B. and Max L. Thomas Cancer Immunology Research Fund, the Charles A. Sammons Cancer Center Research Fund, and the Tri Delta Cancer Research Fund.

² To whom requests for reprints should be addressed, at Cancer Immunology Research Unit, Charles A. Sammons Cancer Center, Baylor University Medical Center, 3500 Gaston Avenue, Dallas, TX 75246.

Received 1/30/89. Revised 4/21/89. Accepted 5/ 3/89.

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