Fariba Akbari Gavabari; Mohsen Rastegari-Pouyani; Saied Afshar; Mehrdokht Mazdeh; Elaheh Talebi-ghane; Mohammad Mahdi Eftekharian
Abstract
Background: Parkinson’s disease (PD) is increasingly recognized as a condition driven by both central and peripheral inflammatory responses, largely mediated by cytokine activity.Objective: To assess IL-35 (P35 and Ebi3 subunits) and IL-37 gene expression, along with the serum levels of IL-35 protein ...
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Background: Parkinson’s disease (PD) is increasingly recognized as a condition driven by both central and peripheral inflammatory responses, largely mediated by cytokine activity.Objective: To assess IL-35 (P35 and Ebi3 subunits) and IL-37 gene expression, along with the serum levels of IL-35 protein in patients with PD compared to healthy controls.Methods: Cytokine gene expression was measured using the qRT-PCR technique, while IL-35 serum levels were measured using the ELISA method. The data obtained were analyzed using a Bayesian regression model in the R software.Results: The results revealed that the expression of P35 gene, of the two subunits of IL-35, did not differ significantly between the two groups. However, Ebi3 and IL-37 transcript levels were significantly lower in patients compared to healthy individuals (p<0.001). In contrast, IL-35 serum level in patients showed a significant increase compared to the control group (p=0.016). Notably, IL-37 expression showed a negative correlation with age (p=0.004). . We also observed positive and significant correlations between the gene expression of P35 and Ebi3 (p= 0.02, r= 0.4), P35 and IL-37 (p= 0.008, r= 0.45), and Ebi3 and IL-37 (p= 0.016, r= 0.41).Conclusion: In conclusion, our study revealed a higher serum protein level of IL-35 in PD patients compared to the healthy control group. Meanwhile, gene expression levels of IL-37 and Ebi-3 were significantly reduced. These alterations in the expression of these cytokines are suggested to be partly responsible for the immune system dysregulation in this disease.
Shirin Torkestani; Alireza Zamani; Mehrdokht Mazdeh; Elahe Talebi-Ghane; Ghodratoallah Roshanaie; Mohammad Mahdi Eftekharian
Abstract
Background: Abnormal humoral and cellular immune responses have been reported in immune-mediated polyneuropathies. CD137, as a costimulatory molecule and a TNF receptor superfamily member, has been demonstrated to have a key role in the pathogenesis of many autoimmune as well as inflammatory disorders.Objective: ...
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Background: Abnormal humoral and cellular immune responses have been reported in immune-mediated polyneuropathies. CD137, as a costimulatory molecule and a TNF receptor superfamily member, has been demonstrated to have a key role in the pathogenesis of many autoimmune as well as inflammatory disorders.Objective: To evaluate the transcripts levels of CD137, its ligand (CD137L), and the serum levels of soluble CD137 (sCD137) in patients with immune-mediated polyneuropathy.Methods: A total of 45 patients and 46 sex and age-matched healthy individuals were enrolled in the study. CD137 and CD137L transcript levels were assessed by the Real-Time PCR, and the serum level of sCD137 was measured using the ELISA technique. The Bayesian regression model was used for statistical analysis at the 0.05 significance level in R 4.1.0 statistical environment. Results: Transcript levels of the CD137 and CD137L were higher in polyneuropathy patients in comparison with the healthy subjects (P=0.006 for both). Conversely, the mean level of sCD137 was significantly lower in the sera of patients compared to the controls (P<0.001).Conclusion: Our findings point to the possible role of CD137 and CD137L in immune-mediated polyneuropathy pathogenesis. More investigations are required to clarify the exact contributions of the mentioned molecules to the pathogenesis of immune-mediated polyneuropathies.
