MiR-3Oa-centered molecular crosstalk regulates STh17 differentiation

Recently,there has been growing interest in the specific role of Th17 cells in the pathogenesis of neuroinflammation-related degenerative diseases,including Alzheimer’s disease(AD),Parkinson’s disease(PD),amyotrophic lateral sclerosis(ALS),and multiple sclerosis(MS)[1].The Th17-mediated autoimmune response is a key determinant of these pathological outcomes.Interleukin-17(IL-17),the most important cytokine of activated Th17 cells,is considered a pivotal agent of autoimmunity because of its proinflammatory effect and migration-promoting ability.Although the specific mechanism of Th17/IL-17 is still controversial,exploring the molecular pathways of Th17/IL-17 in neurodegeneration will facilitate the identification of suitable targets to modulate these cellular processes.Th17 differentiation is directed by lineage-specific transcription factors,including RORγt and RORα,and is controlled by the coordinated activity of a series of positive and negative regulators,as well as additional signals from different cytokines to maintain and stabilize the proinflammatory features of Th17 cells[2,3].