IL-33 Responsive Luciferase Reporter Jurkat Cell Line

The IL-33 Responsive Luciferase Reporter Jurkat Cell Line is a Jurkat cell line engineered to express both human IL33Ra (IL-33 receptor alpha) (NM_016232.5) and human IL1RAP (IL-1 Receptor Accessory Protein) (NM_002182.4) separated by a self-cleaving P2A peptide. The construct was delivered by lentiviral transduction of NF-kappaB Luciferase Reporter Jurkat Cells (#60651), which express a firefly luciferase reporter driven by NF-kappaB (nuclear factor Kappa B) response elements located upstream of the minimal TATA promoter. After activation by IL-33, the endogenous transcription factor NF-kappaB binds to the response elements, inducing transcription of the luciferase reporter gene. This cell line has been validated to respond to IL-33. Figure 1: Illustration of the mechanism of IL-33 Luciferase Reporter Jurkat Cell Line. IL-33 binds to its cognate receptor to activate downstream signal pathways that converge on transcription factor NF-kappaB, which translocates into the nucleus where it can activate the transcription of the Firefly luciferase reporter driven by NF-kappaB response elements present in the promoter. Interested in having us perform the screening and profiling of inhibitors or blocking antibodies? Visit our Immunotherapy Biochemical Screening Services. Interleukin-33 (IL-33) is a tissue-derived alarmin cytokine belonging to the Interleukin-1 (IL-1) family that regulates tissue homeostasis and inflammation and plays a key role in allergic airway diseases. IL-33 is produced constitutively by a variety of cell types, including fibroblasts, endothelial and epithelial cells, where it is stored in the cell nucleus and subsequently released in response to cell necrosis, cellular damage, stress, and tissue injury. After release, IL-33 primarily drives type 2 immune responses by activating TH2 (T helper 2) cells, mast cells, and innate lymphoid cells (ILC2s). IL-33 signals through ST2 (receptor serum-stimulated 2), also known as IL-1RL1, and its co-receptor IL-1RAcP, and activates downstream signaling pathways including NF-kappaB and MAPK (mitogen-activated protein kinase), leading to the production and release of pro-inflammatory cytokines. IL-33 is a promising therapeutic target for inflammatory diseases including asthma and COPD (chronic obstructive pulmonary disease), with anti-IL-33 neutralizing antibodies (including Tozorakimab) currently undergoing clinical trials.