IL-17RE

Interleukin 17 receptor E (IL-17RE) is a specific functional receptor for IL-17C, and primarily expressed by epithelial cells and lymphocytes, such a Th17 cells[1]. IL-17C/IL-17RE-axis plays a role in many inflammatory and immune diseases[2]. Also, no interactions were found between IL-17RE and any of the other IL-17 cytokine family members. IL-17C activated downstream signaling through IL-17RE-IL-17RA complex for the induction of genes encoding antibacterial peptides as well as proinflammatory molecules[3].
Binding of IL-17C to the IL-17RA/RE complex on the epithelial IL-17C-source cells forms an autocrine loop in the epithelium. Like IL-17A, IL-17C signaling through IL-17RA/RE employs the adaptor molecule ACT1. The signaling cascade then activates the MAPK pathway by phosphorylation of p38, ERK, and JNK as well as the NF-κB pathway by phosphorylation of the p65 subunit and the NF-κB inhibitor IκBα[2]. IL-17RE meditates T cell activation, including the expression of effector cytokines (e.g. IL-17A), and the IL-17C/IL-17RE-axis enhances the expression of cytokine by effector Th17 cells in a in a model of autoimmune disease. IL-17RE is also highly expressed by liver resident CD4+ T cells and natural killer T cells and augments T cell function in autoimmune hepatitis together with IL-17C. Deficiency of IL-17RE also provides protection in a model of crescentic nephrotoxic nephritis[1].