Inhibits the activity of interleukin-36 (IL36A,IL36B and IL36G) by binding to receptor IL1RL2/IL-36R and preventing its association with the coreceptor IL1RAP for signaling. Part of the IL-36 signaling system that is thought to be present in epithelial barriers and to take part in local inflammatory response; similar to the IL-1 system with which it shares the coreceptor. Proposed to play a role in skin inflammation. May be involved in the innate immune response to fungal pathogens. May activate an anti-inflammatory signaling pathway by recruiting SIGIRR. Interacts with cargo receptor TMED10; the interaction mediates the translocation from the cytoplasm into the ERGIC (endoplasmic reticulum-Golgi intermediate compartment) and thereby secretion. The secretion is dependent on protein unfolding and facilitated by the cargo receptor TMED10; it results in protein translocation from the cytoplasm into the ERGIC (endoplasmic reticulum-Golgi intermediate compartment) followed by vesicle entry and secretion. Highly abundant in embryonic tissue and tissues containing epithelial cells. Removal of N-terminal methionine is necessary for full antagonistic activity. In combination with transgenic IL36A exacerbates skin abnormalities (acanthosis, hyperkeratosis, presence of a mixed inflammatory cell infiltrate and increased cytokine and chemokine expression). Bioactive (processed) recombinant IL36RN inhibits effects of IL-36 when used in 100- 1000-fold molar excess. Belongs to the IL-1 family. Truncated N-terminus.