IgE and IgG1 production in the type 2 immune response is the characteristic feature of an allergic reaction. However, whether bacterial molecules modulate IgE and IgG1 production remains obscure. Here, we demonstrate that the bacterial quorum sensing molecules acyl homoserine lactones (AHLs) induce IgE and IgG1 production by activating the RARE (retinoic acid response element) response in dendritic cells (DCs) in vivo. DC-specific knockout of the retinoic acid transcriptional factor Rara diminished the AHL-stimulated type 2 immune response in vitro. AHLs altered DC phenotype, upregulated OX40L and IFN-I signature, and promoted T helper 2 cell differentiation in vitro. Finally, AHLs activated the RARE response by inhibiting AKT phosphorylation in vitro, as the AKT agonists IGF-1 and PDGF abolished the effect of AHLs on the RARE response. This study demonstrates a mechanism by which AHLs drive allergic airway inflammation through activating retinoic acid signaling in DCs.

2型免疫反应中IgE和IgG1的产生是过敏反应的特征。但是，细菌分子是否调节IgE和IgG1的产生仍然不清楚。在这里，我们证明了细菌群体感应分子酰基高丝氨酸内酯（AHL）通过激活体内树突状细胞（DC）中的RARE（视黄酸响应元件）响应来诱导IgE和IgG1产生。视黄酸转录因子Rara的DC特异性敲除可减少AHL刺激的2型体外免疫反应。AHL在体外改变DC表型，上调OX40L和IFN-I标记并促进T辅助2细胞分化。最后，AHL通过抑制AKT磷酸化激活RARE反应在体外，由于AKT激动剂IGF-1和PDGF废除了AHL对RARE反应的影响。这项研究证明了AHL通过激活DC中的维甲酸信号来驱动过敏性气道炎症的机制。