Defect in lectin-induced interleukin 2 (IL-2) production by peripheral blood lymphocytes of patients with Hodgkin's disease.

Peripheral blood lymphocytes (PBL) of patients with Hodgkin's disease were studied for their capacity to produce interleukin 2 upon in vitro phytohemaglutinin stimulation in the presence or absence of either interleukin 1 or indomethacin (2 micrograms/ml); eight patients were studied at the discovery of their disease before receiving any therapy (onset HD; OHD). Seventeen patients were tested in long-term (greater than 3 yr) remission (remission HD; RHD); most RHD were treated with both chemotherapy and irradiation. Fourteen healthy individuals served as controls. PBL from OHD have a significant (P less than 0.01) defect in the production of PHA-induced IL-2. Indomethacin and IL-1 had no effect on IL-2 yield. PBL from RHD yield intermediate levels of IL-2, which are nevertheless significantly lower (P less than 0.02) than control values. RHD recover the capacity of normal PBL to increase their production of IL-2 in indomethacin-supplemented culture medium. Interestingly, PHA responsiveness was significantly decreased only in RHD, thus not explaining the low IL-2 yield obtained in supernatants. In addition, 4-day PHA-blasts from both HD patients and control individuals increase their thymidine incorporation in the presence of purified lectin-free IL-2 to a similar degree, suggesting that their IL-2 receptors are unimpaired. Finally, OHD sera significantly inhibit PHA-induced IL-2 yield of normal PBL, suggesting that a seric component(s) may play a role in some cases. We conclude that defective IL-2 production may play a role in the well-documented deficient cellular immunity seen in Hodgkin's disease.