Wiley Interdiscip Rev Syst Biol Med - The role of regulatory T cells in neurodegenerative diseases.

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Resumo

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.

Resumo Limpo

sustain neuroinflammatori respons hallmark mani neurodegen diseas includ parkinson diseas alzheim diseas amyotroph later sclerosi multipl sclerosi hivassoci neurodegener specif subset t cell current recogn foxp cd cd regulatori t cell treg pivot suppress autoimmun maintain immun homeostasi mediat selftoler peripheri shown autoimmun diseas cancer grow bodi evid show treg import maintain immun balanc peripheri also contribut selftoler immun privileg central nervous system articl first review current status knowledg concern develop suppress function treg discuss evid support dysfunct treg sever neurodegen diseas interest dysfunct treg main observ earli stage sever neurodegen diseas chronic stage point causat role inflamm pathogenesi neurodegen diseas furthermor provid overview number molecul hormon neuropeptid neurotransmitt ion channel affect dysfunct treg neurodegen diseas also emphas effect intestin microbiom induct function treg need studi crosstalk enter nervous system treg neurodegen diseas final point need system biolog approach analysi enorm complex regul function treg potenti role neurodegen diseas

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