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WIREs Syst Biol Med
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The role of regulatory T cells in neurodegenerative diseases

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Abstract A sustained neuroinflammatory response is the hallmark of many neurodegenerative diseases, including Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, multiple sclerosis, and HIV‐associated neurodegeneration. A specific subset of T cells, currently recognized as FOXP3+CD25+CD4+ regulatory T cells (Tregs), are pivotal in suppressing autoimmunity and maintaining immune homeostasis by mediating self‐tolerance at the periphery as shown in autoimmune diseases and cancers. A growing body of evidence shows that Tregs are not only important for maintaining immune balance at the periphery but also contribute to self‐tolerance and immune privilege in the central nervous system. In this article, we first review the current status of knowledge concerning the development and the suppressive function of Tregs. We then discuss the evidence supporting a dysfunction of Tregs in several neurodegenerative diseases. Interestingly, a dysfunction of Tregs is mainly observed in the early stages of several neurodegenerative diseases, but not in their chronic stages, pointing to a causative role of inflammation in the pathogenesis of neurodegenerative diseases. Furthermore, we provide an overview of a number of molecules, such as hormones, neuropeptides, neurotransmitters, or ion channels, that affect the dysfunction of Tregs in neurodegenerative diseases. We also emphasize the effects of the intestinal microbiome on the induction and function of Tregs and the need to study the crosstalk between the enteric nervous system and Tregs in neurodegenerative diseases. Finally, we point out the need for a systems biology approach in the analysis of the enormous complexity regulating the function of Tregs and their potential role in neurodegenerative diseases. WIREs Syst Biol Med 2013, 5:153–180. doi: 10.1002/wsbm.1187 This article is categorized under: Biological Mechanisms > Regulatory Biology Translational, Genomic, and Systems Medicine > Therapeutic Methods Translational, Genomic, and Systems Medicine > Translational Medicine

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A schematic figure of important molecules and simplified pathways/mechanisms underlying the suppressive function of Tregs. AKT, v‐akt murine thymoma viral oncogene homolog; D1/5‐R, dopamine type 1 receptor (including D1‐R and D5‐R); FcGRIIB, Fc γ receptor IIB; GAL1/10, Galectin1/10. The other abbreviations are indicated in the text.

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Influence of Tregs on neurodegenerative diseases. (a) Influence of genes or proteins or molecules on Tregs in the murine EAE model. (b) Influence of genes or proteins or molecules on Tregs in patients with RR‐MS. A syringe indicates an administration by injection. 17β‐Estradiol was administrated with pellets. A yellow arrow indicates the consequences of genetic modification or administration or treatment on mice. AII designates octapeptide angiotensin II.

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A simplified diagram showing that the impairment of the suppressive function or the deficiency in differentiation or development of Tregs is inversely correlated with the severity of neurodegenerative diseases.

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Biological Mechanisms > Regulatory Biology
Translational, Genomic, and Systems Medicine > Therapeutic Methods
Translational, Genomic, and Systems Medicine > Translational Medicine

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