Soluble CD23 as an effector of immune dysregulation in chronic uremia and dialysis.

Patients with chronic renal failure often present an immunodeficiency state paradoxically exacerbated by hemodialysis and associated with signs of T cell activation. The presence of circulating monokines suggests that monocytes are also activated. Whether or not this includes B cells is controversial, despite frequently abnormal antibody responses. We thus investigated whether the soluble low-affinity receptor for IgE (Fc epsilon RII/CD23), recently identified as a marker of B cell and monocyte activation and possibly involved in T cell activation, was modulated by chronic renal failure and hemodialysis. Relative to values in healthy individuals (N = 31), plasma concentrations of soluble CD23 were significantly elevated in non-dialyzed chronically uremic patients (N = 44), more elevated in patients on peritoneal dialysis (N = 24), and most elevated in those on regular hemodialysis (N = 132), stabilizing after about six months. Soluble CD23 levels were unmodified by the first dialysis session but rose markedly during regular dialysis with cellulose or polysulfone membranes, but not with polyacrilonitrile AN-69 membranes. Soluble CD23 levels correlated with levels of IgG, and those of tumor necrosis factor alpha and interleukin-6, suggesting that increased sCD23 levels reflect activation of B cells and monocytes, respectively. These findings reinforce the view of soluble CD23 as a multi-functional receptor/cytokine, and provide evidence that it might contribute to the immune dysregulation associated with chronic renal failure and exacerbated by hemodialysis.