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Research Article Free access | 10.1172/JCI109082
Division of Hematology-Oncology, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110
Find articles by Hillinger, S. in: JCI | PubMed | Google Scholar
Division of Hematology-Oncology, Department of Internal Medicine, Washington University School of Medicine, St. Louis, Missouri 63110
Find articles by Herzig, G. in: JCI | PubMed | Google Scholar
Published June 1, 1978 - More info
In Hodgkin's disease a possible mechanism for impaired cellular immunity is cell-mediated suppression, defined as the inhibitory interaction between suppressor cells and effector lymphocytes. To test for the presence of suppressor cells in peripheral blood, we have modified the standard, one-way mixed lymphocyte culture by adding mitomycin C-treated mononuclear cells from the responder. Suppression, expressed as a percent of the base-line mixed lymphocyte culture in which these extra cells are not present, results in a reduction of thymidine incorporated in the modified culture (i.e., 100% suppression = no net thymidine incorporation; 0% suppression = identical thymidine incorporation in both the modified and baseline culture).
Suppression was found to be significantly increased in patients with both active Hodgkin's disease (78±4.6%) and remission Hodgkin's disease (58±9.3%) compared to normal individuals (21±6.9%) (mean±SE). The degree and frequency of suppression were not influenced by disease stage or prior therapy. Cell purification techniques revealed (in 10 patients studied) the suppressor cell to be a monocyte in 6, and a thymus-derived lymphocyte in 4. Possible genetic restriction of the suppressor cell interaction was indicated by a failure of suppressor cells to alter the response of lymphocytes from unrelated individuals, but suppression was obtained with lymphocytes from a histocompatible sibling. Although mononuclear cells from normal individuals suppress less frequently than cells from patients with Hodgkin's disease, normals may demonstrate suppression comparable to that observed in Hodgkin's patients. This finding suggests that suppression is a normal immunoregulatory mechanism which is altered in Hodgkin's disease.