Cutting Edge: The Foxp3 Target miR-155 Contributes to the Development of Regulatory T Cells

被引:313
作者
Kohlhaas, Susan [1 ]
Garden, Oliver A. [2 ,3 ]
Scudamore, Cheryl [4 ]
Turner, Martin [1 ]
Okkenhaug, Klaus [1 ]
Vigorito, Elena [1 ]
机构
[1] Babraham Inst, Lab Lymphocyte Signalling & Dev, Cambridge CB22 3AT, England
[2] Univ London Royal Vet Coll, Dept Vet Clin Sci, Infect & Immun Res Grp, Regulatory T Cell Lab, London, England
[3] Univ London Imperial Coll Sci Technol & Med, Dept Immunol, London, England
[4] Univ London Royal Vet Coll, Dept Pathol & Infect Dis, Hatfield, Herts, England
基金
英国生物技术与生命科学研究理事会; 英国医学研究理事会;
关键词
DICER; DIFFERENTIATION; MICRORNA-155; AUTOIMMUNITY; LINEAGE; ABSENCE; GENES; MICE; REG;
D O I
10.4049/jimmunol.0803162
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Foxp3 is a transcription factor that is essential for the normal development of regulatory T cells (Tregs). In the absence of microRNAs (miRNAs), Foxp3(+) Tregs develop but fail to maintain immune homeostasis, leading to a scurfy-like disease. Global analysis of the network of genes regulated by Foxp3 has identified the miRNA miR-155, which is highly expressed in Tregs, as a direct target of Foxp3. In this study we report that miR-155-deficient mice have reduced numbers of Tregs, both in the thymus and periphery, due to impaired development. However, we found no evidence for defective suppressor activity of miR-155-deficient Tregs, either in vitro or in vivo. Our results indicate that miR-155 contributes to Treg development, but that additional miRNAs control Treg function. The Journal of Immunology, 2009, 182: 2578-2582.
引用
收藏
页码:2578 / 2582
页数:5
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