Anti-Human IL33 Antibody Pair

Product Description: IL-33 is a member of the IL-1 cytokine family and is constitutively expressed in structural and lining cells, such as endothelial and epithelial cells. It acts as an "alarmin" that is released upon cell damage or necrosis to alert the immune system. IL-33 binds to the ST2 receptor, which is expressed on various immune cells including Th2 cells, mast cells, eosinophils, and group 2 innate lymphoid cells (ILC2s). This binding activates signaling pathways like NF-kappaB and MAPK that drive production of type 2 cytokines like IL-5 and IL-13. The IL-33/ST2 pathway plays a critical role in the pathogenesis of allergic and Th2-mediated diseases like asthma, atopic dermatitis, and anaphylaxis. Genetic studies have linked IL-33 and ST2 to increased susceptibility to asthma. Protein Function: Cytokine that binds to and signals through the IL1RL1/ST2 receptor which in turn activates NF-kappa-B and MAPK signaling pathways in target cells (PubMed:16286016, PubMed:19841166). Involved in the maturation of Th2 cells inducing the secretion of T-helper type 2-associated cytokines (PubMed:17853410, PubMed:18836528). Also involved in activation of mast cells, basophils, eosinophils and natural killer cells (PubMed:17853410, PubMed:18836528). Acts as an enhancer of polarization of alternatively activated macrophages (PubMed:19841166). Acts as a chemoattractant for Th2 cells, and may function as an 'alarmin', that amplifies immune responses during tissue injury (PubMed:17853410, PubMed:18836528). Induces rapid UCP2-dependent mitochondrial rewiring that attenuates the generation of reactive oxygen species and preserves the integrity of Krebs cycle required for persistent production of itaconate and subsequent GATA3-dependent differentiation of inflammation-resolving alternatively activated macrophages (By similarity) , In quiescent endothelia the uncleaved form is constitutively and abundantly expressed, and acts as a chromatin-associated nuclear factor with transcriptional repressor properties, it may sequester nuclear NF-kappaB/RELA, lowering expression of its targets (PubMed:21734074). This form is rapidely lost upon angiogenic or pro-inflammatory activation (PubMed:18787100) [The Uniprot Consortium]