Regulation and Interaction among SOCS1 and SOCS3 by MicroRNAs in Multiple Sclerosis: A Review and in Silico Analysis

Multiple sclerosis (MS) is a chronic demyelinating disease and a leading cause of disability in young adults. Its pathophysiology involves complex genetic and immunological mechanisms, among which the suppressors of cytokine signaling (SOCS) proteins play a critical role. These intracellular regulators control cytokine-mediated JAK/STAT signaling, thereby modulating immune activation. In particular, SOCS1 and SOCS3 inhibit key cytokines such as IL-2, IL-12, IL-6, and IL-23, preventing excessive Th1/Th17 responses and neuroinflammation. Dysregulation of SOCS expression or function can favor persistent immune activation and contribute to central nervous system demyelination. MicroRNAs (miRNAs), small non-coding RNAs that repress gene expression post-transcriptionally, have emerged as important modulators of immune regulation. Several miRNAs target SOCS transcripts, influencing their expression and, consequently, cytokine signaling. Altered miRNA profiles have been reported in autoimmune and neurodegenerative diseases, highlighting their potential relevance in MS pathogenesis and as biomarkers. This review summarizes current evidence on SOCS1 and SOCS3 in MS and examines their regulation by miRNAs. In addition, we present a hypothesis-generating in silico analysis identifying candidate miRNAs with predicted interactions with SOCS genes. These computational findings are intended to support and prioritize potential regulatory relationships rather than provide direct experimental validation. Collectively, this integrative approach may offer new insights into disease biology and help guide future experimental studies aimed at identifying biomarkers or therapeutic targets in MS.