Abstract
Acquired immune-mediated polyneuropathies are classified to some subtypes among them are acute and chronic inflammatory demyelinating polyradiculoneuropathies (AIDP and CIDP). These two conditions share some common signs and underlying mechanisms. Based on the roles of Suppressor of cytokine signaling (SOCS) genes in the modulation of immune system reactions, these genes might be involved in the pathogenesis of these conditions. We evaluated expression of SOCS1-3 and SOCS5 genes in the leukocytes of 32 cases of CIDP, 19 cases of AIDP and 40 age- and sex-matched controls using real time PCR method. The Bayesian regression model was used to estimate differences in mean values of genes expressions between cases and control group. Expression levels of SOCS1 and SOCS2 were significantly lower in male patients compared with controls. This sex-specific pattern was also observed for SOCS3 down-regulation. Based on the area under curve values in Receiver Operating Characteristics (ROC) curve, diagnostic powers of SOCS1, SOCS2, SOCS3 and SOCS5 genes in the mentioned disorder were 0.61, 0.73, 0.68 and 0.58, respectively. Expression of none of genes was correlated with age of enrolled cases. The current study shows evidences for participation of SOCS genes in the pathophysiology of acquired immune-mediated polyneuropathies.
Highlights
Immune-mediated neuropathies embrace a variety of peripheral nerve disorders which can be classified according to the course of signs evolution, principal engagement of motor/sensory fibers, dispersal of signs and paraclinical factors [1, 2]
Since Suppressor of cytokine signaling (SOCS) proteins partake in the control of immune cascades, we evaluated expression of SOCS1-3 and SOCS5 genes in the peripheral blood cells of individual affected by immunemediated neuropathies and healthy controls to find their possible role in the pathophysiology of this immune-related condition
Expression levels of SOCS1 and SOCS2 were significantly lower in patients compared with controls (Posterior Beta=-2.18, P=0.029; Posterior Beta=-3.19, P
Summary
Immune-mediated neuropathies embrace a variety of peripheral nerve disorders which can be classified according to the course of signs evolution, principal engagement of motor/sensory fibers, dispersal of signs and paraclinical factors [1, 2]. Two types of these neuropathies are Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) [2]. The pathologic events during evolution of GBS are commonly triggered by environmental factors such as infections or vaccination that stimulate abnormal immune responses, interruption in the blood–nerve barrier and demolition of myelin sheaths and/or axons [4,5,6]. While several studies have highlighted the role of Th1 cells producing proinflammatory cytokines in this condition, some pathogenic events in the GBS cannot be explained by Th1/Th2 imbalance, so other types of T cells such as Th17 and regulatory T cells might been involved in this process [8]
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
