Up‐regulation of miR‐27a promotes monocyte‐mediated inflammatory responses in Kawasaki disease by inhibiting function of B10 cells

Kawasaki disease (KD) is an acute systemic vasculitis and activation of monocytes plays a central role in the pathogenesis of it. B10 cells, a B cell subset with negative regulatory properties, are functionally identified by their ability to express cytoplasmic IL‐10 after ex vivo stimulation. Here, we aimed to explore the functional role of B10 cells during monocyte‐mediated inflammatory responses in KD, as well as elucidate the underlying microRNA (miRNA)‐mediated regulatory mechanisms. Expression of IL‐10 by each group of B cells (total B cells, transitional B cells, naïve B cells, and memory B cells) and inhibition of monocyte‐derived TNF‐α by activated B cells were measured by flow cytometry. Expression of miRNAs (miR‐21‐3p, miR‐98‐5p/3p, miR‐27a‐3p, let7b‐5p, and miR‐1423p/5p) that affect IL‐10 levels in B cells was quantitated by real‐time PCR. The relationship between IL‐10 and these miRNAs was examined by multivariate analysis. MiR‐mediated RNA interference in B cells was performed to investigate the role of miR‐27a on expression of IL‐10. The results showed expression of cytoplasmic IL‐10 in B cell subsets from patients with KD was down‐regulated. The inhibitory effect of B10 cells on production of TNF‐α by monocytes from patients with KD was also compromised. The miR‐27a‐3p expression was markedly up‐regulated during the acute phrase of KD, and it promoted monocyte‐mediated TNF‐α release by negatively regulating expression of cytoplasmic IL‐10 within B cells in vitro. The data suggest up‐regulated miR‐27a in B cells from patients with KD may promote monocyte‐mediated inflammatory responses by inhibiting the regulatory function of B10 cells. Up‐regulated miR‐27a in B cells from patients with KD may promote monocyte‐mediated inflammatory responses by inhibiting the regulatory function of B10 cells .