The IFI16 Knockout Jurkat Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population of the human IFI16 gene in the Jurkat T lymphocyte line. This gene-disrupted model is generated through CRISPR/Cas9-mediated target-gene disruption, yielding a heterogeneous pool of cells carrying loss-of-function mutations in IFI16. The polyclonal format provides a mixed knockout background, advantageous for studies where biological variability informs innate immune signaling and functional screening without requiring clonal isolation.
Jurkat cells are an immortalized T lymphocyte line derived from the peripheral blood of a 14-year-old male with T-cell acute lymphoblastic leukemia. Widely utilized in immunology, they facilitate investigation of T cell receptor signaling, apoptosis, and HIV infection. Their rapid proliferation and genetic tractability make them suitable for CRISPR editing, offering a consistent cellular context for examining gene function within the adaptive immune lineage.
IFI16 functions as an intracellular sensor of cytosolic double-stranded DNA, critical to innate immunity. Upon DNA binding, IFI16 activates STING (TMEM173), triggering TBK1 and IRF3 phosphorylation to induce type I interferons such as interferon-beta and NF-kB-driven cytokines. It also assembles an inflammasome with ASC (PYCARD) and pro-caspase-1, promoting maturation of interleukin-1beta and interleukin-18. IFI16 interacts with p53 to modulate cell cycle arrest and apoptosis, and upstream regulators include type I interferons, DNA virus infection, and cytosolic dsDNA.
In the Jurkat T lymphocyte setting, IFI16 disruption provides a physiologically relevant platform to explore DNA-sensing pathways within cells naturally targeted by viruses like HIV-1. As Jurkat cells retain functional p53, this knockout model enables dissection of IFI16-p53 crosstalk in DNA damage-induced apoptosis, relevant to cancer biology and autoimmune conditions where IFI16 plays a role in SLE and Sjogren’s syndrome.
This model supports diverse experimental applications, including analysis of STING-dependent signaling and inflammasome activation. Validation of IFI16 knockout via Western blot or RT-qPCR can be followed by downstream assays such as phospho-TBK1/phospho-IRF3 immunoblotting, IL-1beta ELISA, Annexin V apoptosis detection, and luciferase-based viral infection studies. It is also suitable for RNA-seq profiling of interferon-stimulated genes, co-immunoprecipitation with STING or ASC, and drug screening for STING pathway modulators. For further information, please contact Ascent Research.
