Similar results were seen in the later phase of hapten-specific IgE-induced skin inflammation: PGD2/DP2/CRTH2 signalling resulted in lymphocyte, eosinophil and basophil infiltration as well as increased levels of macrophage chemokines which was suppressed by DP2/CRTH2 antagonist ramatroban or hPGDS inhibitor HQL-79 [16]. This evidence concerns the gene HPGDS and dermatitis.