The reciprocal interactions between microglia and T cells in Parkinson’s disease: a double-edged sword

Abstract In Parkinson's disease (PD), neurotoxic microglia, Th1 cells, and Th17 cells are overactivated. Overactivation of these immune cells exacerbates the disease process and leads to the pathological development of pro-inflammatory cytokines, chemokines, and contact-killing compounds, causi...

Full description

Bibliographic Details
Main Authors: Yuxiang Xu, Yongjie Li, Changqing Wang, Tingting Han, Haixuan Liu, Lin Sun, Jun Hong, Makoto Hashimoto, Jianshe Wei
Format: Article
Language:English
Published: BMC 2023-02-01
Series:Journal of Neuroinflammation
Subjects:
Online Access:https://doi.org/10.1186/s12974-023-02723-y
_version_ 1811165810919473152
author Yuxiang Xu
Yongjie Li
Changqing Wang
Tingting Han
Haixuan Liu
Lin Sun
Jun Hong
Makoto Hashimoto
Jianshe Wei
author_facet Yuxiang Xu
Yongjie Li
Changqing Wang
Tingting Han
Haixuan Liu
Lin Sun
Jun Hong
Makoto Hashimoto
Jianshe Wei
author_sort Yuxiang Xu
collection DOAJ
description Abstract In Parkinson's disease (PD), neurotoxic microglia, Th1 cells, and Th17 cells are overactivated. Overactivation of these immune cells exacerbates the disease process and leads to the pathological development of pro-inflammatory cytokines, chemokines, and contact-killing compounds, causing the loss of dopaminergic neurons. So far, we have mainly focused on the role of the specific class of immune cells in PD while neglecting the impact of interactions among immune cells on the disease. Therefore, this review demonstrates the reciprocal interplays between microglia and T cells and the associated subpopulations through cytokine and chemokine production that impair and/or protect the pathological process of PD. Furthermore, potential targets and models of PD neuroinflammation are highlighted to provide the new ideas/directions for future research.
first_indexed 2024-04-10T15:42:40Z
format Article
id doaj.art-fb318a636f754309a48bba5b4d49019a
institution Directory Open Access Journal
issn 1742-2094
language English
last_indexed 2024-04-10T15:42:40Z
publishDate 2023-02-01
publisher BMC
record_format Article
series Journal of Neuroinflammation
spelling doaj.art-fb318a636f754309a48bba5b4d49019a2023-02-12T12:18:26ZengBMCJournal of Neuroinflammation1742-20942023-02-0120111410.1186/s12974-023-02723-yThe reciprocal interactions between microglia and T cells in Parkinson’s disease: a double-edged swordYuxiang Xu0Yongjie Li1Changqing Wang2Tingting Han3Haixuan Liu4Lin Sun5Jun Hong6Makoto Hashimoto7Jianshe Wei8Institute for Brain Sciences Research, School of Life Sciences, Henan UniversityDepartment of Rehabilitation Medicine, Beijing Jishuitan Hospital Guizhou Hospital, Guizhou Provincial Orthopedics HospitalInstitute for Brain Sciences Research, School of Life Sciences, Henan UniversityInstitute for Brain Sciences Research, School of Life Sciences, Henan UniversityInstitute for Brain Sciences Research, School of Life Sciences, Henan UniversityHenan Key Laboratory of Polyoxometalate Chemistry, College of Chemistry and Chemical Engineering, Henan UniversityInstitute for Brain Sciences Research, School of Life Sciences, Henan UniversityTokyo Metropolitan Institute of Medical ScienceInstitute for Brain Sciences Research, School of Life Sciences, Henan UniversityAbstract In Parkinson's disease (PD), neurotoxic microglia, Th1 cells, and Th17 cells are overactivated. Overactivation of these immune cells exacerbates the disease process and leads to the pathological development of pro-inflammatory cytokines, chemokines, and contact-killing compounds, causing the loss of dopaminergic neurons. So far, we have mainly focused on the role of the specific class of immune cells in PD while neglecting the impact of interactions among immune cells on the disease. Therefore, this review demonstrates the reciprocal interplays between microglia and T cells and the associated subpopulations through cytokine and chemokine production that impair and/or protect the pathological process of PD. Furthermore, potential targets and models of PD neuroinflammation are highlighted to provide the new ideas/directions for future research.https://doi.org/10.1186/s12974-023-02723-yMicrogliaT cellCell–cell interactionsChemokinesParkinson’s diseaseCytokines
spellingShingle Yuxiang Xu
Yongjie Li
Changqing Wang
Tingting Han
Haixuan Liu
Lin Sun
Jun Hong
Makoto Hashimoto
Jianshe Wei
The reciprocal interactions between microglia and T cells in Parkinson’s disease: a double-edged sword
Journal of Neuroinflammation
Microglia
T cell
Cell–cell interactions
Chemokines
Parkinson’s disease
Cytokines
title The reciprocal interactions between microglia and T cells in Parkinson’s disease: a double-edged sword
title_full The reciprocal interactions between microglia and T cells in Parkinson’s disease: a double-edged sword
title_fullStr The reciprocal interactions between microglia and T cells in Parkinson’s disease: a double-edged sword
title_full_unstemmed The reciprocal interactions between microglia and T cells in Parkinson’s disease: a double-edged sword
title_short The reciprocal interactions between microglia and T cells in Parkinson’s disease: a double-edged sword
title_sort reciprocal interactions between microglia and t cells in parkinson s disease a double edged sword
topic Microglia
T cell
Cell–cell interactions
Chemokines
Parkinson’s disease
Cytokines
url https://doi.org/10.1186/s12974-023-02723-y
work_keys_str_mv AT yuxiangxu thereciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT yongjieli thereciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT changqingwang thereciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT tingtinghan thereciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT haixuanliu thereciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT linsun thereciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT junhong thereciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT makotohashimoto thereciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT jianshewei thereciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT yuxiangxu reciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT yongjieli reciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT changqingwang reciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT tingtinghan reciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT haixuanliu reciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT linsun reciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT junhong reciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT makotohashimoto reciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword
AT jianshewei reciprocalinteractionsbetweenmicrogliaandtcellsinparkinsonsdiseaseadoubleedgedsword