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[Cancer Research 48, 6321-6327, November 15, 1988]
© 1988 American Association for Cancer Research

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Infiltration of Interleukin-2-inducible Killer Cells in Ascitic Fluid and Pleural Effusions of Advanced Cancer Patients

D. Kay Blanchard1, John J. Kavanagh, Joseph G. Sinkovics, Denis Cavanagh, Susan M. Hewitt and Julie Y. Djeu

Departments of Medical Microbiology and Immunology [D. K. B., J. Y. D.] and Oncology [J. J. K., D. C., S. M. H.], University of South Florida College of Medicine and Community Cancer Center, St. Joseph's Hospital [J. G. S.], Tampa, Florida

Using ascitic fluid or pleural effusion obtained from 13 ovarian or metastatic breast cancer patients, we separated tumor cells from effusion-associated lymphocytes (EAL) with Percoll density centrifugation. Lymphocytes were incubated with recombinant interleukin 2 (IL-2) for 3–4 days and then assessed for tumoricidal activity in a 51chromium-release assay. The IL-2-activated EAL were found to lyse autologous fresh tumor cells, as well as allogeneic fresh tumor cells and FMEX tumor cells, a melanoma cell line which is resistant to natural killer cell activity but is sensitive to lysis by lymphokine-activated killer cells. There was little or no tumoricidal activity seen in freshly isolated EAL or in EAL which were cultured in medium without IL-2. Phenotypically, the IL-2-activated EAL were largely CD3-, although some cytolytic activity was found in CD3+ populations. Also, most activity was found in cells positive for CD2 (OKT11) and CD16 (Leu 11b), and negative for the monocyte marker Leu M3. These results indicate that the activated cell types found in EAL were predominantly natural killer/lymphokine-activated killer-like with a small contribution from T-cells. Finally, EAL were readily activated by IL-2 in medium containing autologous effusion fluid, indicating that in situ activation of tumoricidal activity by IL-2 can occur in the face of potentially inhibitory substances or cells that may exist in the effusions. Direct introduction of IL-2 may therefore be a potential therapeutic modality of effusion-forming cancers.

1 To whom requests for reprints should be addressed, at Department of Medical Microbiology and Immunology, University of South Florida College of Medicine, P. O. Box 10, 12901 North 30th Street, Tampa, FL 33612.

Received 5/23/88. Revised 8/16/88. Accepted 8/18/88.




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HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1988 by the American Association for Cancer Research.