Defective cellular immunity in renal failure: depression of reactivity of lymphocytes to phytohemagglutinin by renal failure serum

摘要: Abstract In defining host resistance factors in uremia, experiments were designed to assess the effect of renal failure serum upon reactivity normal human lymphocytes phytohemagglutinin vitro. Normal buffy coat cells resuspended sera obtained from subjects and 14 patients with failure, then stimulated M cellular response measured by increase thymidine or uridine uptake. The mean uptake was 14,389 ±1695 (SEM) cpm per 2 × 106 lymphocytes. Uridine under same conditions 12,540 ±1887 cpm. Compared these are a 2740 ±457 3928 ±667 sera. Both differences significant at P<0.01 level. For controls representing “chronic illnesses,” pneumococcal meningitis, cirrhosis liver without jaundice, rheumatoid arthritis, paraplegia urinary tract infection did not cause suppression. No single drug had been taken all patients; three taking no drugs. The one patient acute suppressed while her after recovery illness supported lymphocyte response. Improvement also noted 9 10 immediately hemodialysis. These observations plus inhibition mixed indicate presence dialyzable inhibitory factor rather than absence supporting sera. Lymphocytes preincubated for 24 hr responded normally when transferred stimulated. Cells within initial incubation demonstrated depressed Also, cell survival 72 as judged trypan blue exclusion chromium-51 release similar Thus, suppressive does depend phytohemagglutinin-cell interaction nor cytotoxic effect. These studies demonstrate that factor(s) can greatly suppress parameter which an immune function circulating is assessed provides least, partial explanation delayed homograft rejections well susceptibility such various infections.