Impaired CD25 expression and soluble CD25-IL-2R alpha receptor release by anti-CD3 stimulated peripheral blood mononuclear cells in Hodgkin's disease patients.

We examined 22 patients in active phase of Hodgkin's disease (HD), 12 patients in complete clinical remission and 16 healthy subjects for their responsiveness to anti-CD3 stimulation as measured by CD25 antigen expression on peripheral blood mononuclear cells (PBMC) and production of CD25-IL-2R alpha. Simultaneously, the serum levels of soluble interleukin 2 receptor alpha (sIL-2R alpha) were estimated. Our studies indicate that PBMC in patients in active phase and in clinical remission have impaired ability to express CD25 antigen after stimulation with anti-CD3 monoclonal antibody. Similarly, the levels of sIL-2R alpha in culture supernatants were significantly lower in both groups of patients: in active phase and clinical remission compared with the controls. In contrast, the mean serum level of sIL-2R alpha was significantly higher in active phase of the disease compared to that found in patients in clinical remission and controls. Our studies suggest that sIL-2R alpha, derived from PBMC, is not the source of increased levels of sIL-2R alpha found in the sera of patients in active phase of HD. Their synthesis and secretion/shedding most probably takes place in the involved tissues.