Interleukin 1 (IL-1) and interleukin 2 (IL-2) production in patients with chronic renal failure

The mechanism of immune deficiency in patients with chronic renal failure (CRF) was investigated by testing both the ability of monocytes to produce IL-1 and the ability of To cells to produce IL-2.IL-1 production by lipopolysaccharide (LPS)-stimulated monocytes from CRF patients was not less than that of healthy controls. In fact, some patients showed higher values than the normal range (mean±2SD of normal value).IL-2 production by phytohemagglutinin (PHA)-stimulated peripheral blood mononuclear cells (PBMC) from patients on hemodialysis was significantly greater than that of healthy controls and non-hemodialysis patients. To exclude the influence of monocytes, the ability of T cells to produce IL-2 was also examined. IL-2 production by PHA-stimulated T cells was also increased in patients on hemodialysis. There was no correlation between IL-2 production by PHA-stimulated T cells and IL-1 production by LPS-stimulated monocytes. These results indicated that the enhanced IL-2 production by T cells was independent of monocytes.The mean IL-1 activity produced by non-stimulated monocytes was less than 1U/ml in all groups. IL-2 production by unstimulated T cells was not observed in any subject. Both the expression of the IL-2 receptor (IL-2R) and that of the transferrin receptor on PBMC were less than 2% at the time cultures were started, or after incubations without stimulation. Thus, the possibility that monocytes and T cells were preactivated could be excluded.There was a significant correlation between IL-2 responsiveness and IL-2R expression on PHA-stimulated PBMC. Both were significantly lower in non-hemodialysis patients than in healthy controls, and gradually improved with the continuation of hemodialysis. One of the causes of immune deficiency, particularly in patients with non-hemodialysis renal failure, might be decreased IL-2 responsiveness based on defective expression of IL-2R.