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Multiple sclerosis (MS) is the most common inflammatory demyelinating disease of the central nervous system (CNS) with various clinical manifestations. The characteristic of MS is that myelin is attacked by the body's immune system and increases the electrical capacity of axons, and is the primary pathophysiological mechanism of the transmission block. Studies have shown that epigenetic factors participate in the development of MS. LncRNAs are highly abundant and heterogeneous linear RNA transcripts with lengths exceeding 200 nucleotides and no protein-coding potential. Currently, pieces of evidence have demonstrated that lncRNAs have fundamental actions in multiple cellular pathways, including immune system regulation, epithelial-mesenchymal transition (EMT), cancer cell growth and metastasis, cellular homeostasis, and embryo development. It has been demonstrated that epigenetic mechanisms have an abundant role in the pathogenesis of MS in which the role of lncRNAs as epigenetic regulatory molecules in molecular processes has been proven. In this paper, we have focused on the correlation between MS and lncRNAs, the role of lncRNA in the pathogenesis of the disease, and the diagnostic and prognostic potential of lncRNA in MS. • The epigenetic factors in the development of MS has recently been considered. • LncRNAs exhibit epigenetic characteristics which may lead to the initiation of MS. • Involvement of LncRNAs in the pathogenesis of MS have been proved. • LncRNAs are involved in the abnormalities immune-related signaling pathways. • Aberrant expression of lncRNAs participates in the advancement of MS via influencing immunological pathways. [ABSTRACT FROM AUTHOR]

Multiple sclerosis (MS) is the most common demyelinating disease which mainly impacts the integrity of central nervous system (CNS). MS etiology is not clearly known but genetic, environmental factors and immune system are the most frequently explored risk factors. Adaptive immune responses have a critical role in MS pathogenesis in which auto-reactive T-cells and autoantibodies are main orchestrators. Immune responses are modulated by inhibitory molecules which regulates adaptive system activation and hemostasis interface. These molecules suppress immune responses through inhibition of cytokine secretion and T cell proliferation and subsequently reducing the inflammation and respective damage. Therefore the critical role of inhibitory molecules in regulating the healthy and safe immune responses make them very attractive target for immunotherapy. In this review paper, the role of inhibitory molecules expressed on the various immune cell types in MS pathogenesis and experimental autoimmune encephalomyelitis (EAE) animal model will be summarized. • VISTA is one of the goals in the therapeutic target for MS treatment. • CTLA-4 polymorphisms do not correlate with MS susceptibility. • Modulating Lag-3 can affect the autoimmune disease as well as MS. • TIM3–galectin-9 pathway associated with auto-reactive T cells. • Modulation of PD1 and PD-L1 pathways holds promise in MS therapeutic potential. [ABSTRACT FROM AUTHOR]