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[Cancer Research 39, 785-792, March 1, 1979]
© 1979 American Association for Cancer Research

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Augmentation of Antitumor Cytotoxicity in MOPC-315 Tumor Bearer Spleen Cells by Depletion of Glass-adherent Cells Prior to in Vitro Activation1

Margalit B. Mokyr2, Donald P. Braun and Sheldon Dray

Department of Microbiology and Immunology, University of Illinois at the Medical Center, Chicago, Illinois 60612

Noncytotoxic, MOPC-315 tumor bearer spleen cells were converted to a cytotoxic state by in vitro activation with MOPC-315 stimulator tumor cells. The level of in vitro cytotoxicity exhibited by activated spleen cells from mice bearing small tumors was similar to that of activated spleen cells from normal mice while that exhibited by activated spleen cells from mice bearing large tumors was much lower. The decrease in the level of in vitro antitumor cytotoxicity observed in activated tumor bearer spleen cells during progressive tumor growth correlated with an increase in the percentage of macrophages in the spleen. Depletion of glass-adherent cells from the spleens of tumor-bearing mice included the removal of most macrophages and resulted in the expression of cytotoxicity upon culture and in the augmentation of cytotoxicity upon activation. Still, unactivated or MOPC-315-activated, nonadherent, tumor bearer spleen cells did not lyse allogeneic EL4 leukemia or syngeneic normal BALB/c target cells. The in vitro cytotoxic activity exhibited by activated, nonadherent, tumor bearer spleen cells against MOPC-315 target cells was at least 10-fold greater than that exhibited by activated normal spleen cells or activated, unfractionated, tumor bearer spleen cells. Furthermore, activated nonadherent, tumor bearer spleen cells were also superior to activated, unfractionated, tumor bearer spleen cells in mediating in vivo antitumor activity in the local adoptive transfer assay. Thus, activated, nonadherent, tumor bearer spleen cells might be useful in immunotherapeutic regimens requiring histocompatible cells with augmented antitumor cytotoxicity.

1 Supported in part by NIH Grant PHS CA-18241.

2 To whom requests for reprints should be addressed.

Received 8/14/78. Accepted 11/20/78.







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 © 1979 by the American Association for Cancer Research.