Regulatory T cells in patients with systemic lupus erythematosus

被引:244
作者
Alvarado-Sanchez, Brenda
Hernandez-Castro, Berenice
Portales-Perez, Diana
Baranda, Lourdes
Layseca-Espinosa, Esther
Abud-Mendoza, Carlos
Cubillas-Tejeda, Ana C.
Gonzalez-Amaro, Roberto
机构
[1] UASLP, Fac Med, Dept Inmunol, San Luis Potosi 78210, SLP, Mexico
[2] UASLP, Fac Ciencias Quim, Lab Inmunol Celular & Mol, San Luis Potosi 78210, SLP, Mexico
[3] Hosp Cent Dr Ignacio Morones Prieto, Unidad Reg Reumatol & Osteoporosis, San Luis Potosi 78210, SLP, Mexico
关键词
autoimmune diseases; systemic lupus erythematosus; treg lymphocytes; suppressor cells;
D O I
10.1016/j.jaut.2006.06.005
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Regulatory T cells have an important role in the control of self-reactivity, and in the pathogenesis of autoimmune inflammatory conditions. The aim of this work was to perform a quantitative and functional analysis of regulatory T cells in patients with systemic lupus erythematosus (SLE). We studied twenty-three patients with SLE (19 active, 4 inactive), and twenty-seven healthy subjects as well as fifteen patients with rheumatoid arthritis (RA). The following cell subsets were analyzed in peripheral blood mononuclear cells by flow cytometry: CD4+CD25+, CD4+CD25(bright), CD4+Foxp3+ (Treg cells), CD8+CD28- (Ts cells), CD4+IL-10+ (Tr1 cells), and CD4+TGF-beta+ (Th3 cells). In addition, the in vitro suppressive activity of CD4+CD25+ lymphocytes was tested. We found no significant differences in the levels of all regulatory cell subsets studied in SLE patients compared to controls and RA patients. However, a defective regulatory function of CD4+CD25+T cells was observed in a significant fraction (31%) of patients with SLE. Our data indicate that although approximately one third of patients with SLE show an abnormal immunosuppressive function of Treg lymphocytes, their levels of the different regulatory T cell subsets in peripheral blood are not significantly different from those found in controls. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:110 / 118
页数:9
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