Anti-IL-36G Antibody

IL-36G is is a member of the interleukin 1 cytokine family whose gene and eight other interleukin 1 family genes form a cytokine gene cluster on chromosome 2 (1) . IL-36G is thought to activate the NF-kappaB pathway through IL-1 receptor family members IL-1RL2 and IL-1RAcP (2) . Like the related proteins IL-36A and IL-36B, IL-36G requires post-translational processing for full agonist activity, but the cleavage mechanism is currently unknown (3) . IL-36G expression is stimulated by interferon-gamma, tumor necrosis factor-alpha and interleukin 1 (4) . The IL-36 cytokines have been suggested to amplify Th1 responses by enhancing proliferation and Th1 polarization of naive CD4+ T cells (5) .

IL-36G antibody was raised against a 13 amino acid peptide near the carboxy terminus of human IL-36G. The immunogen is located within the last 50 amino acids of IL-36G.

Highly expressed in tissues containing epithelial cells: skin, lung, stomach and esophagus. Expressed in bronchial epithelial. In skin is expressed only in keratinocytes but not in fibroblasts, endothelial cells or melanocytes. Up- regulated in lesional psoriasis skin. Expressed in monocyte- derived dendritic cells and M1 macrophages.

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. 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. 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; also stimulates its own expression and that of the prototypic cutaneous proinflammatory parameters TNF-alpha, S100A7/psoriasin and inducible NOS. May play a role in proinflammatory responses during particular neutrophilic airway inflammation: activates mitogen-activated protein kinases and NF-kappa B in primary lung fibroblasts, and stimulates the expression of IL-8 and CXCL3 and Th17 chemokine CCL20 in lung fibroblasts. May be involved in the innate immune response to fungal pathogens, such as Aspergillus fumigatus.