Glucocorticoids increase CD4+CD25high cell percentage and Foxp3 expression in patients with multiple sclerosis

被引：75

作者：

Braitch, M.

Harikrishnan, S.

Robins, R. A. ^{[1
]}

Nichols, C. ^{[2
]}

Fahey, A. J.

Showe, L. ^{[2
]}

Constantinescu, C. S.

机构：

[1] Univ Nottingham, Sch Mol Med Sci, Div Immunol, Nottingham NG7 2UH, England

[2] Wistar Inst Anat & Biol, Syst Biol Div, Genom Core, Philadelphia, PA 19104 USA

来源：

ACTA NEUROLOGICA SCANDINAVICA | 2009年 / 119卷 / 04期

关键词：

CD25; cytokines; Foxp3; glucocorticoids; methylprednisolone; multiple sclerosis; regulatory T cells; REGULATORY T-CELLS; IMMUNOLOGICAL SELF-TOLERANCE; GENE-EXPRESSION; DENDRITIC CELLS; METHYLPREDNISOLONE; RECEPTOR; SUPPRESSION; MECHANISM; THERAPY; RELAPSE;

D O I：

10.1111/j.1600-0404.2008.01090.x

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

To determine whether percentages of CD4(+)CD25(high) T cells (a group of regulatory T cells, Treg) differ in patients with multiple sclerosis (MS) in relapse vs remission after glucocorticoid treatment and whether treatment for relapses changes Treg population and the expression of Foxp3, a key Treg-associated molecule. Peripheral blood mononuclear cells (PBMC) were obtained from 20 patients with MS during relapse, just before and 2 days after starting steroid treatment (i.v. methylprednisolone 1 g/day for 3 days) and then 6 weeks after treatment. CD4(+)CD25(hi) cells were analysed by using flow cytometry. Cytokines were measured by using an ELISA and Foxp3, CD3 and CD25 expression by using quantitative real-time PCR. The percentage of CD4(+)CD25(hi) cells, plasma IL-10 and Foxp3/CD3 ratio increased 48 h after methylprednisolone initiation and returned to baseline values by 6 weeks post-treatment. Results suggest that glucocorticoids increase Treg cell functional molecules and percentages. This may be a mechanism whereby steroids expedite recovery from MS relapses.

引用

页码：239 / 245

页数：7

共 31 条

[1] Foxp3 interacts with nuclear factor of activated T cells and NF-κB to repress cytokine gene expression and effector functions of T helper cells [J].