Journal of Okayama Medical Association
Published by Okayama Medical Association

Full-text articles are available 3 years after publication.


吉永 泰彦 岡山大学医学部第三内科学教室
Thumnail 100_483.pdf 5.52 MB
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 T 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 lU/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.