Il17re, the Interleukin-17 receptor E, is part of the IL-17 receptor family. This family is involved in signal transduction pathways that play a crucial role in protecting the host against extracellular pathogens but also contribute to inflammatory pathology in autoimmune diseases [1]. The IL-17 cytokines bind to their receptors, including Il17re, to initiate intracellular signaling, which is involved in multiple biological processes such as inflammation regulation. Genetic models, like gene knockout (KO) or conditional knockout (CKO) mouse models, are valuable for studying Il17re's functions.

In an ApcMin mouse model colonized with enterotoxigenic Bacteroides fragilis, the Bacteroides fragilis toxin triggers a pro-carcinogenic, multi-step inflammatory cascade that requires Il17re, NF-κB, and Stat3 signaling in colonic epithelial cells. This shows that Il17re is involved in the process of microbe-induced colon tumorigenesis [2]. In the KC-Tie2 inflammatory dermatitis mouse model, genetic elimination of Il17re, along with Il17c and Il17ra, reversed the increases in IL-17C and Zc3h12a and improved the skin phenotype, indicating its role in self-sustaining skin inflammation [3].

In conclusion, Il17re is essential in regulating inflammation-related biological processes. The KO/CKO mouse models have revealed its significance in diseases such as colon tumorigenesis and skin inflammation. These findings contribute to understanding the role of Il17re in disease mechanisms, potentially guiding the development of new therapeutic strategies for related diseases.