The major findings are briefly summarized as follows: 1) the EP2 receptor is required for PGE2-enhanced IgE production by B cells; 2) EP2-mediated signal increases IgE production by facilitating IL-4-induced STAT6 activation and transcription of downstream targets critical for IgE class switching; 3) PGE2 signaling through EP2 promotes antigen-specific IgE responses in vivo and contributes to the development of OVA-induced asthma. Here, IL4 is linked to asthma.