Altered IL-23/IL-17A immune axis in Parkinson's disease: An exploratory analysis

Parkinson's disease (PD) is a progressive neurodegenerative disorder with a multifactorial basis. Immune dysregulation, both in the periphery and the brain, has been suggested to contribute to neurodegeneration in PD. Recent research has suggested a crucial role of T lymphocytes, especially the Th17 lineage, in α-synuclein-mediated neurodegenerative disorders. Whether Th17 cells exhibit pathogenic potential in PD is not adequately known. In this study, the role of cytokines that regulate the commitment, development, pathogenic transformation, and effector function of Th17 cells was examined in patients with PD.

This case-control study was conducted on 46 patients with PD and an equal number of age and sex-matched healthy controls (HC). The serum levels of five Th17-pathway-related cytokines, such as IL-1β, IL-6, TNF-α, IL-23, and IL-17A, were measured in all the study participants by Multiplex Suspension Assay. The serum cytokine levels were compared between patients with PD and HC.

Serum levels of IL-6 (p < 0.001), IL-23 (p < 0.001), TNF-α (p = 0.027), and IL-17A (p = 0.004) were significantly elevated in patients with PD compared to HC. Importantly, IL-6 levels showed a significant positive correlation with TNF-α, IL-23, and IL-17A levels, while IL-23 levels positively correlated with the levels of IL-17A.

The findings suggest elevated levels of inducer, mediator, and effector cytokines of the inflammatory Th17 cells in PD. Furthermore, the significant positive correlation between IL-23 and IL-17A suggests an activated IL-23/IL-17A immune axis in PD.