Athologic Th17 responses for the duration of autoimmune inflammation, controlling IL-1, IL-6, and IL-23 cytokines [152]. Mice with miR-223p-knockout exhibited reduced numbers of myeloid DCs and Th17 cells in the CNS, thereby decreasing EAE illness severity linked to decreased inflammation [152]. Besides, miR-223 is required for efficient macrophage M2 polarization, and mice lacking miR-223 show impaired CNS remyelination [153]. Based on the type of regulated pathway, miR-233-3p exhibits anti- and pro-inflammatory properties. Around the one hand, Li et al. demonstrated that miR-223-3p modulates the noncanonical NF-B (nuclear factor-B) pathway by targeting transcripts of the inhibitor of kappa B SW155246 Autophagy kinase alpha (IKK) (engaged in activation of NF-B), which can be an anti-inflammatory aspect that could protect against the spontaneous activation of macrophages, therefore promoting controlled inflammation inside the human myeloid leukemia cell line [154]. Alternatively, miR-2233p, by targeting TNF receptor-associated aspect six (TRAF6) and TGF- activated kinase 1 binding protein 1, suppresses the canonical NF-B pathway. Therefore, miR-223-3p expression was indicated to decrease neutrophil activation, suggesting anti-inflammatory effects [155]. In addition, Chen et al. demonstrated that miR-223-3p straight targets the transcription factor signal transducer and activator of transcription three (STAT3). It was shownInt. J. Mol. Sci. 2021, 22,11 ofthat miR-223-3p overexpression was linked having a important reduce in STAT3 levels and reduction inside the production of IL-1 and IL-6, but not TNF-, in macrophages. Thereby, miR-223-3p may well regulate processes connected using the regulation of inflammatory responses in macrophages [156]. Moreover, miR-223-3p could downregulate the nod-like receptor pyrin domain containing 3 (NLRP3), which can be believed to become a important and vital factor in MS development. Decreasing the NLRP3 level inhibits inflammation by means of caspase-1 and IL-1, as a result minimizing brain edema and improving neurological functions [15759]. In addition to, miR-223-3p appears to market neuronal protection Cilnidipine-d7 Inhibitor partly by way of the regulation of glutamate receptor signaling. Glutamate receptor two and N-methyl D-aspartate receptor 2B expressions are subunits for glutamate’s ionotropic transmembrane receptors that mediate rapid synaptic transmission in the CNS. It was demonstrated that miR-223-3p overexpression in the retina and optic nerve, by reducing the expression with the above subunits, had blocked the formation of EAE-driven pathological axonal swellings, that are attributed to excitotoxicity of glutamate [160,161]. It was investigated that miR-326-5p downregulates the expression of transcription element Ets-1 [162], a damaging regulator of Th17 differentiation, thereby advertising Th17 differentiation. MiR-326-5p expression is closely correlated with disease severity, both in individuals with MS and mice with EAE [162]. Nonetheless, the exact function of Ets-1 in regulating the differentiation and function of Th17 cells nevertheless remains unknown [163]. In one more study, Honardoost et al. also confirmed the possible of miR-326-5p, obtained from peripheral blood lymphocytes, as a diagnostic biomarker to discriminate among relapsing and remitting phases of MS illness [164]. Research performed on phosphatase and tensin homolog-induced kinase 1 (PINK1)-deficient mice suggest that miR-326 may upregulate GFAP expression for the duration of neural stem cells’ (NSCs) differentiation and brain development [165]. In add.