Itch, also known as pruritus, is the uncomfortable sensation that triggers the desire to scratch. It is transmitted via histaminergic and nonhistaminergic pathways through G protein-coupled receptors and transient receptor potential channels, playing a crucial role in the complex interplay between the immune and neural systems [1,3]. The study of Itch using gene knockout (KO) or conditional knockout (CKO) mouse models can provide valuable insights into its function in vivo.

In atopic dermatitis, mouse models have shown that a lowering of the itch threshold, at least in part due to the increase in intraepidermal nerve fibers and sensory nerve sensitization by interleukin-33 from keratinocytes, leads to a vicious itch-scratch cycle. Type 2 cytokines secreted by Th2 cells further sensitize itch, highlighting the role of Itch in this skin disorder [2].

In conclusion, Itch is essential in the sensation of itch and its associated pathological conditions such as atopic dermatitis. KO/CKO mouse models have been instrumental in revealing its role in the development and progression of these diseases, contributing to our understanding of the underlying mechanisms and potentially guiding the development of new treatments.