Plasticity of Treg cells: Is reprogramming of Treg cells possible in the presence of FOXP3?

被引:15
作者
Beyer, Marc [1 ]
Schultze, Joachim L. [1 ]
机构
[1] Univ Bonn, Lab Genom & Immunoregulat, LIMES Inst, D-53115 Bonn, Germany
关键词
Regulatory T cells; FOXP3; Plasticity; TRANSCRIPTION FACTOR FOXP3; ROR-GAMMA-T; DNA METHYLATION; CUTTING EDGE; TARGET GENES; TGF-BETA; DIFFERENTIAL REQUIREMENT; SUPPRESSIVE FUNCTION; IN-VIVO; EXPRESSION;
D O I
10.1016/j.intimp.2010.11.024
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Regulatory T cells (T-reg cells) are involved in self tolerance, immune homeostasis, prevention of autoimmunity, and suppression of immunity to pathogens or tumors. The forkhead transcription factor FOXP3 is essential for Leg-cell development and function as mutations in FOXP3 cause severe autoimmune diseases in mice and humans. Over the last years it has been postulated that FOXP3 expression in T-reg prevents effector T-cell (T-effector-cell) lineage commitment, yet several recent studies suggest that the co-existence of effector and regulatory T-cell programs can occur and might help to enable Treg cells with properties necessary to exert their function in peripheral tissues. Furthermore, downregulation of FOXP3 in the periphery might help Treg cells to lose suppressive functions and gain memory properties with specificity for self-antigens and an effector phenotype including the ability to produce IFN-gamma and IL-17. This plasticity might have an impact on their reactivity towards autoimmunity as well as tumors or infections. (C) 2010 Elsevier B.V. All rights reserved.
引用
收藏
页码:555 / 560
页数:6
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