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Identification of a Novel CD56^- Lymphokine-activated Killer Cell Precursor in Cancer Patients Receiving Recombinant Interleukin 2¹

Section of Hematology/Oncology, Loyola University Stritch School of Medicine, Maywood, Illinois 60153

Circulating lymphokine-activated killer (LAK) cell activity in cancer patients receiving recombinant interleukin 2 (rIL-2) therapy is confined to cells expressing the CD56 surface marker. However, CD56^- cells from these patients but not normal individuals have been reported to exhibit LAK cytotoxicity only following in vitro activation with rIL-2. Studies were performed to document the existence of CD56^- LAK precursor cells and to phenotypically characterize this population in patients receiving rIL-2 therapy using fluorescence-activated cell sorter-purified CD56^- cell subsets. Initial studies confirmed that CD56^- cells exhibit NK activity [20 ± 7 (SE) LU/10⁶ cells] but not LAK activity (0 ± 0 LU/10⁶ cells) when evaluated directly from peripheral blood of patients receiving rIL-2. CD56^- cells from patients but not normal individuals developed significant LAK cytolytic activity against NK-resistant COLO 205 targets (16 ± 3 LU/10⁶ cells) when cultured for 3 days with 1500 units/ml rIL-2. The CD56^- LAK precursor activity was confined to cells expressing a CD56^-CD16⁺ phenotype and a large granular lymphocyte morphology; little or no NK or LAK precursor activity was detectable in CD56^-CD5⁺ T-cells from patients. Phenotypic characterization of CD16⁺CD56^- cells revealed that this population is uniformly CD11a⁺, CD18⁺, and CD38⁺ and is heterogeneous in its expression of CD11b, CD11c, and CD16/Leu 11c. These results indicate that rIL-2 administration induces enhanced LAK precursor activity in a novel population of CD5^-CD16⁺CD56^- cells.

¹ Supported by Grant CA48069 from the National Cancer Institute.

² To whom requests for reprints should be addressed, at Section of Hematology/Oncology, Loyola University School of Medicine, 2160 South First Avenue, Maywood, IL 60153.

Received 6/ 8/92. Accepted 9/11/92.

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