Role of suppressor cells in depression of T lymphocyte proliferative response in untreated and treated Hodgkin's disease.
The present study was undertaken to elucidate the type and the role of suppressor cells on T lymphocyte response to PHA in untreated and treated patients with Hodgkin's disease. The mean value of peripheral blood T lymphocyte response to PHA in untreated or treated patients was lower than that in healthy subjects. However, the difference was not statistically significant. There was no significant difference in T lymphocyte response between localized and generalized stage or between different cell types in both active and remission Hodgkin's disease patients. The mean T lymphocyte response to PHA of active patients without systemic symptoms (A), on the other hand, was significantly higher than that of active patients with systemic symptoms (B). The mean value of T lymphocyte response in the presence of monocyte-enriched E- cells was significantly lower, whereas the mean value in the presence of monocyte-depleted E- cells was only moderately lower than that in the absence of these non-T cells in active patients. The mean value of PHA response of T lymphocytes with monocyte-enriched or monocyte-depleted E- cells was only slightly lower than PHA response without these cells in remission patients. No suppressor cell activity of T cells was observed in both active and remission patients. The only significant difference in the suppressor cell activity of monocyte-enriched E- cells on the T lymphocyte response to PHA was observed between localized and generalized stage in patients with active disease. Unlike peripheral blood monocyte-enriched E- cells, the splenic monocyte-enriched E- cells possessed no significant suppressor cell activity on the splenic T lymphocyte response to PHA in active Hodgkin's disease patients. These observations suggest that the depression of in vitro cell-mediated immunity seen in patients with active Hodgkin's disease may be due to the non-specific suppression of T lymphocyte response by monocytes, in addition to a possibly intrinsic defect of T lymphocytes.
D000328:Adult; D002469:Cell Separation; D006689:Hodgkin Disease / Q000276:immunology* / Q000473:pathology; D006801:Humans; D008213:Lymphocyte Activation; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology; D009367:Neoplasm Staging; D010835:Phytohemagglutinins / Q000276:immunology / Q000494:pharmacology; D013601:T-Lymphocytes / Q000276:immunology*; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*
D010835:Phytohemagglutinins