Detection and Significance of TypeⅠIFN Receptor on the Treg Cells from Patients with Systemic Lupus Erythematosus_West China Medical Journal

Authors：

SUN Wencui ¹ ,  YAN Bing ² , SHI Guixiu ² , HE Yan ¹ , SUN Yuechi ²

1. State Key Laboratory of Biotherapy;2. Department of Rheumatology; West China Hospital， Sichuan University, Chengdu, Sichuan 610041, P. R. China;

Corresponding author：

YAN Bing, Email: wencui2009@126.com

Keywords：

系统性红斑狼疮; 调节性T细胞; Ⅰ型干扰素受体; 疾病活动指数

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目的　检测系统性红斑狼疮（SLE）患者CD4+CD25+调节性T细胞（Treg）上Ⅰ型干扰素受体（IFNAR）的分布格局，了解Ⅰ型干扰素对SLE患者CD4+CD25+Treg产生直接影响的作用靶点。方法　选取2010年9月－2011年10月间20例初次确诊的SLE患者（SLE组）和20例健康女性（对照组），分离SLE患者和对照组的外周血单个核细胞，采用流式细胞术测定CD4+CD25+Treg上IFNAR的表达。结果　① IFNAR1、IFNAR2在Treg和CD4+CD25? T细胞表面均有表达；两组Treg表面IFNAR1和IFNAR2的表达水平均高于CD4+CD25? T细胞。② 与对照组相比，SLE组Treg表面IFNAR1表达的平均荧光强度明显增高（P=0.001）。③ SLE组Treg表面IFNAR1表达平均荧光强度与疾病活动指数评分呈正相关（rs=0.505，P=0.023）。结论　SLE患者CD4+CD25+Treg表面相对高表达IFNAR1且与疾病活动性相关，提示Ⅰ型干扰素以Treg上IFNAR为靶点在SLE发病机制中可能发挥重要作用，为SLE等自身免疫性疾病治疗寻找新的干预手段提供了理论基础。

Citation： SUN Wencui,YAN Bing,SHI Guixiu,HE Yan,SUN Yuechi. Detection and Significance of TypeⅠIFN Receptor on the Treg Cells from Patients with Systemic Lupus Erythematosus. West China Medical Journal, 2012, 27(6): 823-827. doi: Copy

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1. 　Chen Y, Cuda C, Morel L. Genetic determination of T cell help in loss of tolerance to nuclear antigens[J]. J Immunol, 2005, 174(12): 7692-7702.
2. 　Yan B, Ye S, Chen G, et al. Dysfunctional CD4+, CD25+ regulatory T cells in untreated active systemic lupus erythematosus secondary to interferon-alpha-producing antigen-presenting cells[J]. Arthritis Rheum, 2008, 58(3): 801-812.
3. 　Banchereau J, Pascual V. TypeⅠinterferon in systemic lupus erythematosus and other autoimmune diseases[J]. Immunity, 2006, 25(3): 383-392.
4. 　Blanco P, Palucka AK, Gill M, et al. Induction of dendritic cell differentiation by IFN-alpha in systemic lupus erythematosus[J]. Science, 2001, 294(5546): 1540-1543.
5. 　Santiago-Raber ML, Baccala R, Haraldsson KM, et al. Type-Ⅰinterferon receptor deficiency reduces lupus-like disease in NZB mice[J]. J Exp Med, 2003, 197(6): 777-788.
6. 　Nacionales DC, Kelly-Scumpia KM, Lee PY, et al. Deficiency of the typeⅠinterferon receptor protects mice from experimental lupus[J]. Arthritis Rheum, 2007, 56(11): 3770-3783.
7. 　Foster GR, Masri SH, David R, et al. IFN-α subtypes differentially affect human T cell motility[J]. J Immunol, 2004, 173(3): 1663-1670.
8. 　Pascual V, Farkas L, Banchereau J. Systemic lupus erythematosus: all roads lead to typeⅠinterferons[J]. Curr Opin Immunol, 2006, 18(6): 676-682.
9. 　Ronnblom L, Eloranta ML, Alm GV. The typeⅠinterferon system in systemic lupus erythematosus[J]. Arthritis Rheum, 2006, 54(2): 408-420.
10. 　Barrat FJ, Meeker T, Gregorio J, et al. Nucleic acids of mammalian origin can act as endogenous ligands for Toll-like receptors and may promote systemic lupus erythematosus[J]. J Exp Med, 2005, 202(8): 1131-1139.
11. 　Savarese E, Chae OW, Trowitzsch S, et al. U1 small nuclear ribonucleoprotein immune complexes induce typeⅠinterferon in plasmacytoid dendritic cells through TLR7[J]. Blood, 2006, 107(8): 3229-3234.
12. 　Vollmer J, Tluk S, Schmitz C, et al. Immune stimulation mediated by autoantigen binding sites within small nuclear RNAs involves Toll-like receptors 7 and 8[J]. J Exp Med, 2005, 202(11): 1575-1585.
13. 　Means TK, Latz E, Hayashi F, et al. Human lupus autoantibody-DNA complexes activate DCs through cooperation of CD32 and TLR9[J]. J Clin Invest, 2005, 115(2): 407-417.

West China Medical Journal

Detection and Significance of TypeⅠIFN Receptor on the Treg Cells from Patients with Systemic Lupus Erythematosus

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