Human Interleukin-33 (IL36A) is a cytokine that binds to and signals through the IL1RL2/IL-36R receptor, which in turn activates NF-kappa-B and MAPK signaling pathways in target cells linked to a pro-inflammatory response. 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 IL1RAP. It seems to be involved in skin inflammatory response by acting on keratinocytes, dendritic cells and indirectly on T-cells to drive tissue infiltration, cell maturation and cell proliferation. In cultured keratinocytes induces the expression of macrophage, T-cell, and neutrophil chemokines, such as CCL3, CCL4, CCL5, CCL2, CCL17, CCL22, CL20, CCL5, CCL2, CCL17, CCL22, CXCL8, CCL20 and CXCL1, and the production of proinflammatory cytokines such as TNF-alpha, IL-8 and IL-6. In cultured monocytes upregulates expression of IL-1A, IL-1B and IL-6. In myeloid dendritic cells involved in cell maturation by upregulating surface expression of CD83, CD86 and HLA-DR. In monocyte-derived dendritic cells facilitates dendritic cell maturation and drives T-cell proliferation. It may play a role in pro-inflammatory effects in the lung.

Full-length mature form of human IL36A cDNA (6 – 158aa) was constructed with codon optimization gene synthesis and expressed with a human Alpha Fetal protein N-terminal-His-TEV cleavage site Tag (217aa) fusion at AFP N-terminal. This protein was expressed in E. coli as inclusion bodies. The final product was refolded using our unique “temperature shift inclusion body refolding” technology and chromatographically purified.

1. May be used for in vitro IL36A mediated NF-kappa-B and MAPK signaling pathways regulation study in various cells with this protein either as soluble factor or as coating matrix protein.