Downregulation of SOCS1 gene in the development of Guillain-Barré syndrome
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Date
2023-12Publisher
Brac UniversityAuthor
Khurshid, SarahMetadata
Show full item recordAbstract
Guillain-Barre syndrome (GBS), is a post-infectious disorder of the peripheral nervous system
mediated by an aberrant immune response where cytokines play an imperative role in disease
pathogenesis. Suppressor of cytokine signaling (SOCS1) proteins, a classical inhibitor of the JAKSTAT
signaling pathway, which regulates down-regulates cytokine signaling and suppresses
autoimmunity. Therefore, we aimed to determine the association of SOCS1 protein gene expression
with GBS immunopathogenesis. This prospective study included 33 GBS patients and 33 healthy
controls (HC) in Bangladesh. Detailed clinical investigations and blood samples were collected.
Expression of SOCS1 gene was determined by qPCR and measured by using the 2−ΔCT method.
Mann-Whitney U-test was performed to measure statistical difference of the 2−ΔCT values among
the case and controls. The Pearson correlation was performed to find the association of SOCS1
mRNA expression with the response of regulatory T cells (Tregs) in GBS and healthy individuals.
The median age of patients was 31 years (IQR: 22–40), with male predominance (65%). 69% of
patients had antecedent events, mostly diarrhea (60 %), and 33% were severely affected. We found
significant downregulation of SOCS1 mRNA expression in GBS patients compared to HCs
(median: 0.7582 vs. 1.198, P = 0.0463). We also found a statistically insignificant trend of decrease
in the expression of SOCS1 mRNA in severe GBS patients compared to mild GBS (median=0.7582
vs. 2.370). However, there were no significant associations between SOCS1 gene expressions and
other clinical manifestations of GBS. In addition to that, no significant correlation was found
between SOCS1 mRNA expression and CD4+CD25+Tregs, CD4+FOXP3+Tregs, and
CD4+CD25+FOXP3+Tregs cell responses in patients with GBS and HCs. Thus, downregulation of
the SOCS1 gene may play a pivotal role in developing this autoimmunity in patients with GBS. A
large sample size is required to validate the association of the SOCS1 gene with GBS pathogenesis
and further clinical progression of the disease.