Therefore, the reduction of filaments and other barrier related molecules in the Th2-deviated environment, as well as the deficiency of AhR ligands, may underlie the skin lesions in AD (117), which may compensate for the up-regulation of AhR/ARNT signal transduction pathways to weaken the occurrence of Th2 type response mediated skin inflammation. This evidence concerns the gene AHR and dermatitis.