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The role of Th17 cells/IL-17A in AD, PD, ALS and the strategic therapy targeting on IL-17A
Neurodegenerative diseases are a group of disorders characterized by progressive loss of certain populations of neurons, which eventually lead to dysfunction. These diseases include Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). Immune pathway dysregulat...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9034482/ https://www.ncbi.nlm.nih.gov/pubmed/35459141 http://dx.doi.org/10.1186/s12974-022-02446-6 |
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author | Fu, Jiajia Huang, Yan Bao, Ting Liu, Chengcheng Liu, Xi Chen, Xueping |
author_facet | Fu, Jiajia Huang, Yan Bao, Ting Liu, Chengcheng Liu, Xi Chen, Xueping |
author_sort | Fu, Jiajia |
collection | PubMed |
description | Neurodegenerative diseases are a group of disorders characterized by progressive loss of certain populations of neurons, which eventually lead to dysfunction. These diseases include Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). Immune pathway dysregulation is one of the common features of neurodegeneration. Recently, there is growing interest in the specific role of T helper Th 17 cells and Interleukin-17A (IL-17A), the most important cytokine of Th 17 cells, in the pathogenesis of the central nervous system (CNS) of neurodegenerative diseases. In the present study, we summarized current knowledge about the function of Th17/IL-17A, the physiology of Th17/IL-17A in diseases, and the contribution of Th17/IL-17A in AD, PD, and ALS. We also update the findings on IL-17A-targeting drugs as potentially immunomodulatory therapeutic agents for neurodegenerative diseases. Although the specific mechanism of Th17/IL-17A in this group of diseases is still controversial, uncovering the molecular pathways of Th17/IL-17A in neurodegeneration allows the identification of suitable targets to modulate these cellular processes. Therapeutics targeting IL-17A might represent potentially novel anti-neurodegeneration drugs. |
format | Online Article Text |
id | pubmed-9034482 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-90344822022-04-24 The role of Th17 cells/IL-17A in AD, PD, ALS and the strategic therapy targeting on IL-17A Fu, Jiajia Huang, Yan Bao, Ting Liu, Chengcheng Liu, Xi Chen, Xueping J Neuroinflammation Review Neurodegenerative diseases are a group of disorders characterized by progressive loss of certain populations of neurons, which eventually lead to dysfunction. These diseases include Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS). Immune pathway dysregulation is one of the common features of neurodegeneration. Recently, there is growing interest in the specific role of T helper Th 17 cells and Interleukin-17A (IL-17A), the most important cytokine of Th 17 cells, in the pathogenesis of the central nervous system (CNS) of neurodegenerative diseases. In the present study, we summarized current knowledge about the function of Th17/IL-17A, the physiology of Th17/IL-17A in diseases, and the contribution of Th17/IL-17A in AD, PD, and ALS. We also update the findings on IL-17A-targeting drugs as potentially immunomodulatory therapeutic agents for neurodegenerative diseases. Although the specific mechanism of Th17/IL-17A in this group of diseases is still controversial, uncovering the molecular pathways of Th17/IL-17A in neurodegeneration allows the identification of suitable targets to modulate these cellular processes. Therapeutics targeting IL-17A might represent potentially novel anti-neurodegeneration drugs. BioMed Central 2022-04-22 /pmc/articles/PMC9034482/ /pubmed/35459141 http://dx.doi.org/10.1186/s12974-022-02446-6 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Review Fu, Jiajia Huang, Yan Bao, Ting Liu, Chengcheng Liu, Xi Chen, Xueping The role of Th17 cells/IL-17A in AD, PD, ALS and the strategic therapy targeting on IL-17A |
title | The role of Th17 cells/IL-17A in AD, PD, ALS and the strategic therapy targeting on IL-17A |
title_full | The role of Th17 cells/IL-17A in AD, PD, ALS and the strategic therapy targeting on IL-17A |
title_fullStr | The role of Th17 cells/IL-17A in AD, PD, ALS and the strategic therapy targeting on IL-17A |
title_full_unstemmed | The role of Th17 cells/IL-17A in AD, PD, ALS and the strategic therapy targeting on IL-17A |
title_short | The role of Th17 cells/IL-17A in AD, PD, ALS and the strategic therapy targeting on IL-17A |
title_sort | role of th17 cells/il-17a in ad, pd, als and the strategic therapy targeting on il-17a |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9034482/ https://www.ncbi.nlm.nih.gov/pubmed/35459141 http://dx.doi.org/10.1186/s12974-022-02446-6 |
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