MicroRNA-155 modulates P2R-signaling and Th2-priming of dendritic cells during allergic airway inflammation in mice

MicroRNA-466a-3p attenuates allergic nasal inflammation in mice by targeting GATA3

“…MiR-155 deficiency alleviates allergic airway inflammation in mice by diminishing Th2 priming capacity and ATP-/ P2R-induced activation of dendritic cells [23]. The upregulation of miR-19a in asthma may be an indicator and a cause of increased TH2 cytokine production in the airways [24].…”

MicroRNA‐155: microtuning the allergic concert

“…provide further insights on the molecular mechanisms of miR‐155 activity in allergic airway inflammation, by showing a novel cross talk of miR‐155 and ATP‐type 2 purinergic receptors (P2R) signaling in DCs (Fig. ) . It has been previously reported that extracellular ATP, released into the airways, contributes to the initiation and maintenance of allergic airway inflammation via signaling through P2R on DCs .…”

“…In the current issue of Allergy , Zech et al. provide evidence that miR‐155 is essential in DCs for the initiation and maintenance of allergic airway inflammation. Using a DC‐driven murine model, it was demonstrated that miR‐155 deficiency in DCs resulted in a marked decrease in common features of allergic airway inflammation, that is, airway eosinophilia, production of Th2‐cytokines, peribronchial inflammation, and a reduced bronchial hyper‐responsiveness.…”

“…Now, Zech et al. performed an in silico prediction of miR‐155 targets and identified potential binding sites of miR‐155 on Entpd1 and Entpd3 , members of the ectonucleotidase family responsible for ATP degradation. In accordance, Entpd1 and Entpd3 expression levels were upregulated in lung tissue and DCs of miR‐155 −/− mice, which presented an increased local ATPase activity compared to wild‐type animals.…”

Recent developments and highlights in allergic rhinitis

“…The deficiency of miRNA-155 can alleviate allergic airway inflammation by reducing Th2 immune reaction and ATP-/P2R-induced activation of dendritic cells in mice, which suggests that miRNA-155 is a potential therapeutic target for allergic airway disease. 28,29 The levels of miR-92b, miR-210, and miR-34a in airway epithelial extracellular vesicles are significantly correlated with lung function parameters in children, and lower miRNA levels in nasal lavages are associated with airway obstruction. 30 Epigenetic changes in AR patients, including up-or down-regulation of DNA methylation and microRNA levels, may be potential treatment targets in the future.…”