Alexiewicz J M, Gaciong Z, Klinger M, Linker-Israeli M, Pitts T O, Massry S G
Department of Medicine, University of Southern California School of Medicine, Los Angeles.
Am J Nephrol. 1990;10(6):495-501. doi: 10.1159/000168175.
Previous studies in our laboratory showed that the T cell is a target for parathyroid hormone (PTH) action. It is theoretically possible, therefore, that chronic exposure of the T cells to high blood levels of PTH in patients with chronic renal failure may adversely affect T cell function. We examined in both normal subjects and dialysis patients several aspects of T cell function, including (1) T cell proliferation in response to phytohemagglutinin (PHA) mitogen with and without PTH and with and without exogenous interleukin 2 (IL-2); (2) the IL-2 production induced by PHA with and without PTH, and (3) resting levels of cytosolic calcium--[Ca2+]i--and the increment in [Ca2+]i in response to anti-CD3 antibody. Although PHA significantly (p less than 0.01) stimulated proliferation of T cells from both normal subjects and dialysis patients, the magnitude of the stimulation was significantly (p less than 0.01) smaller in the latter group. In both normal subjects and dialysis patients, exogenous IL-2 alone stimulated T cell proliferation, and the magnitude of the stimulation was similar to that produced by PHA. Also, IL-2 augmented PHA-induced proliferation of T cells from normal subjects, but failed to do so in T cells from dialysis patients. PHA did not augment IL-2 production by T cells from dialysis patients, and PTH did not correct this defect. The resting levels of [Ca2+]i in T cells from dialysis patients were significantly (p less than 0.01) higher, and the increments in [Ca2+]i in response to anti-CD3 antibody were significantly (p less than 0.01) lower than in T cells from normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
