TLR7 (Toll-like receptor 7)/NF-kappaB Luciferase Reporter HEK293 Cell Line

The TLR7 (Toll-like receptor 7)/NF-kappaB Luciferase Reporter HEK293 Cell Line is a HEK293 cell line that expresses the Firefly luciferase reporter under the control of NF-kappaB (nuclear factor kappaB) response element, human TLR7 (Toll-like receptor 7) (NM_016562.4), and a mutated version of the chaperone protein UNC93B1 (inc-93 homolog B1) (NM_030930.4), to obtain a fully active NF-kappaB signaling pathway upon TLR7 stimulation. This cell line has been validated with CL307, R848, KT474, Zimlovisertib and Edecesertib. The family of Toll-like receptors (TLRs) are cell surface receptors that detect a wide variety of microbial components and elicit innate immune responses. Toll-like receptor 7 (TLR7), however, is primarily located in endosomes. TLR7 signaling supports human systemic autoimmune diseases, such as systemic lupus erythematosus (SLE). Patients with SLE display phenotypes that are consistent with increased TLR7 signaling associated with elevated IgD-CD27 double-negative B cells. The TLR7 signaling pathway starts with the binding of ligands like single-stranded RNA from viruses, and the receptor is transported to lysosome-related organelles, a process that involves chaperone proteins like UNC93B1. Adapters such as MyD88 recruit proteins that eventually activate the transcription factors NK-kappaB (nuclear factor kappaB) and IRF7 (Interferon Regulatory Factor 7). Signaling through Toll-like receptor 7 (TLR7) drives the production of type I IFN (interferon) and promotes the activation of auto-reactive B cells. TLR7 inhibition has been proposed as a therapeutic approach for SLE and other autoimmune diseases.