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Department of Microbiology and Immunology, UCLA School of Medicine, University of California at Los Angeles, Los Angeles, California 90024
The reticulum cell sarcoma (RCS) tumor in SJL/J mice has been shown to stimulate a strong syngeneic proliferative response. A unique characteristic of the RCS tumor is that it requires host T-cells for growth. Consequently, factors that inhibit host T-cell proliferation may have a profound effect on tumor cell growth in vivo. This report investigates the relationship between a serum inhibitor of T-cell proliferation and tumor growth. Inhibition was measured in an interleukin 2-dependent proliferation of the CTLL-2 line. Sera from mice with RCS transplantable lines or from mice with spontaneous tumors were much less inhibitory than were sera from normal syngeneic SJL/J mice or from allogeneic mice. The inhibitory activity appears to follow a circadian rhythm, because serum derived in the morning was more inhibitory than was serum derived in the evening. Serum from female mice was less inhibitory than serum from male mice. In contrast to male mice, serum from 35-week-old female mice was as inhibitory as was that from young (8- to 12-week-old) mice. The mechanism of serum inhibition in tumor-bearing mice was examined. The serum was tested for the presence of interleukin 2 which could decrease inhibitory activity, and no interleukin was found. Furthermore, absorption of the serum with CTLL-2 cells did not enhance the inhibitory effect to the level of normal mouse serum. These results suggest that tumor growth in vivo coincides with less serum inhibitor, providing an adequate T-cell response requisite for tumor growth. This corroborates the notion of RCS-host T-cell interaction necessary for tumor growth which is in part regulated by a serum inhibitor.
1 Supported by Grant CA 19753 awarded by the National Cancer Institute. To whom requests for reprints should be addressed.
Received 7/27/84. Revised 12/ 4/84. Accepted 12/31/84.
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