Foxp3, Regulatory T Cell, and Autoimmune Diseases

Inflammation
Jin-Hui TaoXiang-pei Li

Abstract

Regulatory T cells (Tregs) represent a cell type that promotes immune tolerance to autologous components and maintains immune system homeostasis. The abnormal function of Tregs is relevant to the pathogenesis of systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and other autoimmune diseases. Therefore, therapeutic modulation of Tregs could be a potent means of treating autoimmune diseases. Human Tregs are diverse, however, and not all of them have immunosuppressive effects. Forkhead box P3 (Foxp3), a pivotal transcription factor of Tregs that is crucial in maintaining Treg immunosuppressive function, can be expressed heterogeneously or unstably across Treg subpopulations. Insights into modulating Treg differentiation on the level of DNA transcription or protein modification may improve the success of Treg modifying immunotherapies. In this review, we will summarize three main prospects: the regulatory mechanism of Foxp3, the influence on Foxp3 and Tregs in autoimmune diseases, then finally, how Tregs can be used to treat autoimmune diseases.

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Methods Mentioned

BETA
ubiquitination
acetylation
deubiquitination
protein modification

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