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Nephrology Dialysis Transplantation, Vol 14, Issue 1 49-55, Copyright © 1999 by Oxford University Press


RAPID COMMUNICATIONS

Effect of renal dialysis therapy modality on T cell cytokine production

A Zamauskaite, I Perez-Cruz, M Yaqoob, J Madrigal and S Cohen
The Anthony Nolan Bone Marrow Trust, The Department of Haematology, The Royal Free Hospital, Pond Street, London, UK; The Renal Unit, St Bartholomew's Hospital, London, UK; Corresponding author at: The Anthony Nolan Bone Marrow Trust, The Royal Free Hospital, Pond Street, Hampstead, London NW3 2QG, UK

Introduction: Dialysis has been associated with acute changes in the complement activation status, granulocyte markers, macrophage function, T cell activation and the release of pro-inflammatory cytokines. The most common analysis of cytokine production in patients in dialysis has focused on the changes in monokines (particularly IL-1 and TNF&agr;), however it is becoming clear that T cell cytokines play a major role in the impaired lymphocyte function of dialysis patients. Methods: To assess the effect of dialysis modality on T cell function we analysed the ability of T cells within peripheral blood mononuclear cell populations (PBMC) to produce cytokines after mitogen (phorbol-12-myristate-13-acetate; PMA and Ionomycin; I) stimulation in patients on peritoneal dialysis (PD) compared to low flux haemodialysis (HD) and normal individuals (controls). Results: In control PBMC, PMA + I stimulation significantly increased the percentage of CD3+ cells expressing IL-2, IFN&ggr;, TNF&agr;, IL-4 and IL-10, as expected. However, although mitogen stimulation significantly enhanced the percentage of the classical Th1 cytokines (IL-2, IFN&ggr; and TNF&agr;) in the low flux HD PBMC, it had no effect on CD3+ IL-2 or CD3+ TNF&agr; producing cells in the PD group. In contrast, the percentage of T cells producing Th2 cytokines (IL-4 and IL-10) could not be consistently enhanced by mitogen in either dialysis group. Conclusions: We suggest that PD alters the ability of T cells to produce cytokines, possibly by causing an 'exhaustion' of Th1 cells, thereby preventing cells to produce cytokine on ex vivo stimulation. Furthermore, since T cells from both low flux HD and PD groups cold not be induced to produce Th2 cytokines we suggest that uraemia or dialysis per se inhibits T cells from producing the Th2 cytokines. Key words: dialysis, Th1, Th2, intracellular cytokines
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