Abstract
To investigate the mechanism of immunologic defects in uremia, we examined the cell-mediated immunity in 20 uremic patients with well balanced dietary assessments before continuous ambulatory peritoneal dialysis (CAPD) therapy and the serial changes in cell-mediated immunity 3, 6, 9, and 12 months after therapy. Absolute lymphocyte count, active T, total T, OKT4, OKT8, and B-cell levels were significantly lower in uremic patients than in controls, but progressively increased after CAPD treatment. The lymphoproliferative responses to mitogens decreased and were more evidently suppressed in the presence of autologous plasma. The suppressive effect of autologous plasma could be abolished by indomethacin treatment. The plasma prostaglandin E2 level, which was increased in uremic patients, decreased after CAPD treatment. These results suggest that prostaglandin E2 may play an important role in the suppression of T-cell function. The T-cell response to the stimulation of autologous non-T cells (autologous mixed-lymphocyte reaction; AMLR) in uremic patients was also low in patients before CAPD treatment. The patients’ autoreactive T cells could suppress AMLR, and so did the supernatant from AMLR and isolated T-cell culture of uremic patients. These results suggest the existence of suppressor autoreactive T cells which can release suppressor factor(s). However, to our surprise, the autoreactive T-cell proliferation increased, and the suppressive effect of the supernatant was abolished after CAPD therapy. The mechanism for this peculiar phenomenon is not known and deserves further investigation. The suppression effect of the supernatant suggests that a serum factor may also be involved. The beneficial effect of CAPD on immune impairment of uremic patients was further demonstrated by the progressive improvement in interleukin 2 and r-interferon production, natural killer cell activity, and AMLR response after CAPD treatment. It is possible that CAPD can remove the serum inhibitory factors).