PLCE1 and contact dermatitis: For example, PLCε−/− mice homozygous for the inactivated PLCε allele exhibited markedly attenuated inflammatory responses in various disease models including the dextran sulfate sodium (DSS)-induced inflammatory colitis, phorbor ester-induced skin inflammation, contact dermatitis and bronchial asthma models8–13, and, moreover, transgenic mice overexpressing PLCε in skin keratinocytes spontaneously developed chronic skin inflammation resembling human psoriasis14.