IRF Reporter (Luc) THP-1 Cell Line

Description

IRF Reporter (Luc) THP-1 Cell Line is a genetically engineered human monocytic cell line designed to monitor interferon regulatory factor (IRF) signaling pathway activation through luciferase (Luc) reporter expression. Derived from THP-1 cells, it maintains key native THP-1 characteristics, such as the capacity to upregulate CD14 upon differentiation and PMA-induced differentiation into macrophage-like cells while featuring a luciferase reporter system under the control of IRF-responsive elements. The cell line enables sensitive quantification of innate immune responses through bioluminescence measurement, making it particularly valuable for studying viral infection responses, TLR signaling, and interferon production. Cells exhibit dose-dependent luciferase activity upon IRF pathway activation while retaining their original biological properties, allowing for high-throughput screening of immunomodulatory compounds. Maintained at low passage numbers (<P20) to ensure reporter stability and consistent performance, this cell line provides a reliable tool for immunology and virology research. The cells are rigorously tested to ensure they are free of contamination from HIV-1, HBV, HCV, Syphilis, mycoplasma, Fungi, Yeast and Bacteria.

Application

• FOR RESEARCH USE ONLY
  

• The IRF Reporter (Luc) THP-1 Cell Line is a genetically engineered human monocytic model designed to monitor interferon regulatory factor (IRF) signaling pathway activation through luciferase reporter expression. This system enables sensitive, quantitative detection of innate immune responses to viral infection, TLR agonists, or STING pathway activation via bioluminescence imaging. The cell line provides dynamic readouts for studying interferon signaling, antiviral immunity, and autoimmune disorders while maintaining THP-1’s differentiation capacity. Maintain in RPMI-1640 with 10% FBS and selection antibiotics to ensure stable reporter performance during investigations of type I interferon responses.