摘要
Impaired suppressive function of CD4+CD25high regulatory T cells (Treg) has been reported as a novel pathogenetic mechanism in Multiple sclerosis (MS). We addressed if high apoptosis sensitivity of MS-Treg could explain this functional Treg defect. Treg from treatment-naïve MS patients showed high sensitivity towards CD95Ligand-mediated apoptosis and exhibited enhanced cell death to IL-2 and TCR-signal deprivation. Since susceptibility of Treg to cell death was similar in MS patients and healthy controls, this cannot explain the inhibitory dysfunction of Treg associated with MS. Furthermore, as cell death is not enhanced, therapeutic expansion of MS-Treg in vitro should be a reasonable and novel therapeutic option.