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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]

• We comment on work by Schinkelshoek et al "H1N1 hemagglutinin-specific HLA-DQ6 restricted CD4+ T cells can be readily detected in narcolepsy type 1 patients and healthy controls. " in J. Neuroimmunology • These authors found no evidence of mimicry between flu hemagglutinin (HA) and Hypocretin (HCRT) • Referring to a paper by Luo et al. Proc. Natl. Acad. Sci. 115(52): E12323-E12332, 2018, we report that by sequencing 100 times more cells we do in fact find evidence for cross reacting TCR sequences, suggesting mimicry. [ABSTRACT FROM AUTHOR]