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The reciprocal interactions between microglia and T cells in Parkinson's disease: a double-edged sword
Yuxiang Xu1,2, Yongjie Li3, Changqing Wang1
1Institute for Brain Sciences Research, School of Life Sciences, Henan University, Kaifeng, 475004, China.
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.
Insights
Parkinson's disease involves overactivated immune cells like microglia, Th1, and Th17 cells. This review explores their interactions, revealing how these cell communications influence Parkinson's disease progression and neuroinflammation.
Area of Science:
- Neuroimmunology
- Neurodegenerative Diseases
- Parkinson's Disease Pathogenesis
Background:
- Overactivation of microglia, Th1 cells, and Th17 cells contributes to Parkinson's disease (PD) pathology.
- Pro-inflammatory cytokines and chemokines released by these cells exacerbate neuronal damage and dopaminergic neuron loss.
- Previous research has largely focused on individual immune cell roles, overlooking crucial inter-cellular interactions in PD.
Purpose of the Study:
- To review the reciprocal interactions between microglia and T cell subpopulations in Parkinson's disease.
- To elucidate how these immune cell communications, via cytokine and chemokine signaling, impact PD progression.
- To highlight potential therapeutic targets and models for PD neuroinflammation.
Main Methods:
- Literature review synthesizing current research on immune cell interplay in PD.
- Analysis of cytokine and chemokine profiles associated with microglia-T cell interactions.
- Identification of key molecular pathways involved in PD neuroinflammation.
Main Results:
- Microglia and T cells (Th1, Th17) exhibit complex reciprocal interactions in PD.
- These interactions, mediated by specific cytokines and chemokines, can both impair and protect against PD pathology.
- The balance of these interactions significantly influences neuroinflammation and dopaminergic neuron survival.
Conclusions:
- Understanding microglia-T cell crosstalk is critical for comprehending PD pathogenesis.
- Targeting these immune cell interactions offers novel therapeutic strategies for Parkinson's disease.
- Further research into PD neuroinflammation models and targets is warranted.
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