Indicating that BAFF/BAFF-R interactions were involved in B cells survival. Altogether, this work provides a mechanistic explanation to the control of BAFF transcripts expression and demonstrates that cytokine secretion by resident cells of target organs of autoimmune diseases can be negatively regulated at the post-transcriptional level by miRNAs. A tentative model describing these interactions is depicted in Figure 2S. The understanding of these complex pathways has important implications for the development of future therapeutic applications. Indeed, the success of Belimumab in the treatment of patients with RA and ongoing clinical trials in SSc suggest that therapeutic targeting of BAFF could be of interest. Our present study suggests that miR-30a-3p mimic could be used to target BAFF mRNA in autoimmune diseases. Recently, patients chronically infected with hepatitis C virus treated with locked nucleic acid against miR-122 showed a prolonged dose-dependent Paclitaxel abmole bioscience reductions in HCV RNA levels without evidence of viral resistance, which suggests that miRNA modulation in patients could become a new therapeutic option in the future. There is a fundamental distinction between acute and chronic inflammation in various pathological studies. Acute inflammation comprises the immediate and early response to an injurious agent and is basically a defensive response that paves the way for repair of the damaged site. The term “neuroinflammation” is appropriate where limited neuronal insults trigger glial cell activation. Neuroinflammation revolves around direct neuro-glial cell responses which are induced by infection and injury within the CNS. It also involves the mechanism by which these responses ultimately contribute to neuropathology and neurobiology of diseases. Microglia are the resident macrophage-like population in the central nervous system. Microglia remain quiescent in the CNS, unable to perform effector and APC functions until activated by injury or infection, and have been suggested to represent the first line of defence for the CNS, which normally lacks professional APCs until they are recruited to the CNS by inflammatory stimuli. Previous studies demonstrated that microglia can be persistently infected by neurotropic strains of Mouse hepatitis virus. Neurotropic MHV infection in mice causes meningoencephalitis, myelitis, and demyelination associated with pronounced activation of microglia. This is evident from characteristic changes in microglial cellular morphology and presence of abundant phagocytotic microglia in demyelinating plaques. MHV-induced CNS injury during early stage of infection involves microglia mediated neuroinflammation. But the mechanism by which these inflammatory responses ultimately contribute to MHV-induced demyelination and axonal loss is not clear. To understand neuroinflammatory pathways, expression of host inflammatory genes in MHV-infected mouse spinal cord.