The Open Autoimmunity Journal


ISSN: 1876-8946 ― Volume 6, 2014

CD4+/FOXP3+ Regulatory T Cells in End-Stage Kidney Disease: Molecular Pathways Trough Cell-Cycle Arrest and Apoptosis

The Open Autoimmunity Journal, 2009, 1: 37-44

Pascal Meier

Service of nephrology, Department of internal medicine, CHCVs Hôpital de Sion and University of Lausanne, Switzerland

Electronic publication date 21/5/2009
[DOI: 10.2174/1876894600901010037]


CD4+/FOXP3+ regulatory T cells (Tregs) are essential for the maintenance of self-tolerance, and Tregs deficiency results in spontaneous autoimmunity in both mice and humans. The forkhead box P3 (FOXP3) expression is required for both survival of Tregs precursors as well as their function. This suggests that Tregs may use multiple mechanisms to limit autoimmunity, and may reflect functional heterogeneity among Tregs subsets that localize to distinct tissue environments. Both cell contact- and cytokine-based immunosuppressive mechanisms would require that Tregs be in close proximity to their targets. The fundamental regulatory activity that can be consistently demonstrated by Tregs in vivo and in vitro has stimulated great interest in developing novel strategies for treating ongoing inflammatory conditions. Patients with end-stage kidney disease (ESKD) are known to display a cellular immune dysfunction. Uremic solutes that accumulate during ESKD may be involved in these processes. In these patients, oxidative stress induced by oxidized LDL (oxLDL) may increase Tregs sensitivity to Fas-mediated apoptosis in part as a consequence of 26S proteasome activation. The 26S proteasome, an ATP-dependent multisubunit protease complex found in the cytoplasm and in the nucleus of all eukaryotic cells, constitutes the central proteolytic machinery of the ubiquitin/proteasome system. Considering the effect of uremia and oxLDL, Tregs from patients with ESKD exhibit early cell-cycle arrest and become apoptotic. These phenomena are the consequence of the oxLDL inhibited proteasome proteolytic activity of p27Kip1 and Bax proteins in Tregs. This may be one mechanistic explanation of the cellular immune dysfunction in patients with ESKD, and may have important implications in clinics, since this response could contribute to the micro-inflammation and atherogenesis encountered in this population.

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