miR-23b-3p deficiency exacerbates immune dysregulation in immunoglobulin A vasculitis by enhancing TLR4-mediated dendritic cell activation - PubMed
5 hours ago
- #miR-23b-3p
- #IgA vasculitis
- #TLR4
- miR-23b-3p deficiency worsens immune dysregulation in IgA vasculitis (IgAV) by enhancing TLR4-mediated dendritic cell (DC) activation.
- IgAV rats showed increased TLR4 expression and reduced miR-23b-3p levels in peripheral blood and spleen tissues.
- miR-23b-3p directly targets TLR4 to suppress its expression, influencing DC maturation and function.
- Overexpression of miR-23b-3p in vivo improved IgAV symptoms by reducing TLR4 expression on DCs, decreasing T follicular helper (Tfh) cell differentiation, and lowering serum IgA, IL-6, and IL-12 levels.
- TLR4 silencing reversed the effects of miR-23b-3p inhibition, normalizing DC activation and Tfh cell differentiation.
- The study suggests miR-23b-3p restoration as a potential therapeutic strategy for IgAV by modulating the DC-Tfh axis via TLR4.