Glucocorticoid treatment restores the impaired suppressive function of regulatory T cells in patients with relapsing-remitting multiple sclerosis

Abstract

Glucocorticoid treatment restores the impaired suppressive function of regulatory T cells in patients with relapsing–remitting multiple sclerosiscei_3987 26..30 L. Xu,* Z. Xu† and M. Xu* *Department of Neurosurgery, Daping Hospital, and †Department of Neurology, Daping Hospital, Third Military Medical University, PLA, Chongqing, China Summary Patients relapsing from multiple sclerosis (MS) are treated with high-dose, short-term intravenous injection of glucocorticoid (GC), although its mecha- nism of action remains only partly understood. We evaluated the ex vivo and in vitro effects of GC on regulatory T cell (Treg) function in 14 relapsing– remitting MS (RR-MS) patients in acute phase and 20 healthy controls (HC). Treg function was enhanced significantly after 5 days of GC treat- ment. Furthermore, there was a trend towards increasing proportions of CD4+CD25+forkhead box P3+ T cells and interleukin-10 secretion with GC treatment when compared with HC. In conclusion, GC treatment restores the impaired Treg function in patients with RR-MS in its acute phase. Keywords: FoxP3, glucocorticoid, IL-10, multiple sclerosis, regulatory T cells Accepted for publication 11 June 2009 Correspondence: M. Xu, Department of Neurosurgery, Daping Hospital, Third Military Medical University, PLA, Chongqing 400042, China. E-mail: xuminhui1960@hotmail.com There is no conflict of interest of any anthors in relation to this submission. Introduction Multiple sclerosis (MS) is an inflammatory, demyelinating disease of the central nervous system (CNS), believed to be initiated and mediated by autoreactive T cells directed against myelin antigens [1]. The development of autoim- mune disease implies a breakdown of the mechanisms that control self-reactive lymphocytes [2,3]. Recent data suggest that such control mechanisms entail a subset of regulatory T cells (Tregs) enriched in the naturally activated CD4+ T cells and that express the CD25 molecule constitutively [3]. Tregs are pivotal agents i

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