Recombinant Mouse IL36G

Background

IL36G, another member of the IL-1 family, functions as a potent pro-inflammatory cytokine by signaling through the IL-36 receptor (IL1RL2) and IL1RAP, leading to activation of NF-κB, ERK, and MAPK pathways. IL36G is highly expressed in epithelial cells, particularly in the skin, lungs, and gastrointestinal tract, where it acts as an amplifier of local inflammation. It induces the production of cytokines, chemokines, and antimicrobial peptides, enhancing the recruitment of immune cells like T cells, dendritic cells, and neutrophils to barrier tissues during infection, injury, or inflammatory insults. IL36G plays a critical role in psoriasis pathogenesis, where it triggers keratinocyte proliferation and immune cell infiltration, contributing to chronic inflammation and skin remodeling. Dysregulated IL36G expression is also associated with respiratory diseases and inflammatory bowel disease. Knockdown studies show impaired immune cell recruitment and weakened epithelial responses, highlighting IL36G's role as an inflammation driver, immune amplifier, and barrier tissue regulator.