This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Catalona, W. J. Articles by McCool, R. E. Search for Related Content PubMed PubMed Citation Articles by Catalona, W. J. Articles by McCool, R. E.

Concanavalin A-inducible Suppressor Cells in Regional Lymph Nodes of Cancer Patients¹

The Yalem Research Laboratories of The Jewish Hospital of St. Louis, Department of Surgery, Washington University School of Medicine, St. Louis, Missouri 63110

Regional tumor-draining lymph nodes of 11 of 14 patients with urological tumors and one of four controls studied contained suppressor cell precursors that could be activated by concanavalin A (Con A) to suppress the proliferative response of autologous lymphocytes to Con A. In contrast, no suppression of lymphocyte proliferation by lymph node cells that were not activated with Con A was observed in four patients tested. The suppressive effect was not due to decreased viability or increased release of cold thymidine by Con A-activated cells nor to alteration in the time course of the proliferative response of Con A-activated cells. Mitomycin C treatment of lymph node cells 24 hr after activation did not abrogate their suppressive activity. Peak suppression was observed after 72 hr in culture. The amount of suppression measured could be maximized by treatment of suppressor cells with mitomycin C 24 hr after activation and by washing the cells immediately before pulse labeling with tritiated thymidine. The concentration of Con A required to produce peak suppression varied from patient to patient with optimal doses ranging from 5 to 25 µg/ml.

¹ This investigation was supported in part by Grant 1 R26 CA23855-01, awarded by the National Cancer Institute, Department of Health, Education, and Welfare, Washington University Biomedical Research Grant 3375-55874-B, General Research Support Grant RIA-N50104-0 from The Jewish Hospital of St. Louis, and American Cancer Society Institutional Research Grant 1N36Q.

² Recipient of American Cancer Society Junior Faculty Clinical Fellowship 382. To whom requests for reprints should be addressed, at Washington University School of Medicine, 4960 Audubon Avenue, St. Louis, Mo. 63110.

Received 8/23/78. Accepted 8/ 2/79.