Background
Neuroinflammation has been proved to play a role in dopaminergic neuronal death in Parkinson’s disease (PD). This link highlights the relevance of the immune response in the progression of the disease. However, little is known about the impact of peripheral immune response on the disease. This study is aimed to evaluate how immune cell populations change in untreated PD patients followed-up for 2 years.
Methods
Thirty-two patients with no previous treatment (PD-0 yr) and twenty-two healthy subjects (controls) were included in the study. PD patients were sampled 1 and 2 years after the start of the treatment. CD4 T cells (naïve/central memory, effector, and activated), CD8 T cells (activated, central memory, effector memory, NKT, Tc1, Tc2, and Tc17), and B cells (activated, plasma, and Lip-AP) were characterized by flow cytometry.
Results
We observed decreased levels of naïve/central memory CD4 and CD8 T cells, Tc1, Tc2, NKT, and plasma cells, and increased levels of effector T cells, activated T cells, and Tc17.
Conclusions
PD patients treated for 2 years showed an imbalance in the naive/effector immune response. Naïve and effector cell levels were associated with clinical deterioration. These populations are also correlated to aging. On the other hand, higher Tc17 levels suggest an increased inflammatory response, which may impact the progression of the disease. Our results highlight the relevant effect of treatment on the immune response, which could improve our management of the disease.
While several studies have been conducted on the immune cell populations in systemic lupus erythematosus (SLE) and Parkinson's disease (PD) patients, very few works have focused on the relationship between both diseases. Being a purely autoimmune disease, SLE is known to exhibit high levels of proinflammatory cells. On the other hand, neuroinflammation is a key contributor to the death of dopaminergic neurons in PD. Herein, we report the case of a patient suffering from both SLE and PD, comparing it with a patient suffering from PD only. Our results are informative, showing decreased levels of regulatory populations like CD8+regs and functional Bregs in the SLE/PD patient. In contrast, the levels of tolerogenic dendritic cells were up to 10 times higher in this patient. Additionally, the levels of Tr1, Th3, and functional CD8 cells, as well as those of M2-like monocytes, were higher in the SLE/PD patient. Regarding the inflammatory response, increased levels of total CD8+ T cells and CD40-expressing DCs were observed. In conclusion, significant changes in the levels of immune cell populations were observed in a patient suffering from SLE and PD, suggesting that the immune response could impact the pathophysiology of PD.
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