The IFIT3 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Jurkat human T lymphocyte cell line, featuring targeted disruption of the IFIT3 gene. This product provides a genetically modified pool of cells lacking functional IFIT3 expression, enabling loss-of-function studies in a well-defined immunological background without clonal selection.
The Jurkat cell line is an established model derived from a human T cell leukemia, widely employed to investigate T cell receptor (TCR)/CD3 signaling, interleukin-2 (IL-2) production, and leukemia biology. These suspension-adapted cells exhibit characteristic TCR-dependent activation cascades, making them suitable for studying signal transduction events relevant to adaptive immunity and hematological malignancies.
IFIT3 is an interferon-stimulated gene with potent antiviral functions. It binds viral RNA and suppresses translation, thereby restricting viral replication. Mechanistically, IFIT3 is induced by type I (IFN-??/??) and type II (IFN-??) interferons via JAK-STAT signaling, requiring IRF9, STAT1, and STAT2. Upstream regulators include IRF3, IRF7, and NF-??B, while downstream interactions involve MAVS, STING, and the IFIT1/2 complex. IFIT3 also bridges RIG-I/MDA5 signaling to caspase-mediated apoptosis, connecting innate immunity to cell death.
In the Jurkat context, knockout of IFIT3 disrupts interferon-driven antiviral responses and may alter apoptotic thresholds. This model reveals IFIT3??s role in T cell-intrinsic innate immunity, where it modulates responses to viral double-stranded RNA. Given Jurkat??s utility in studying leukemia and immune signaling, the knockout cells provide a platform to dissect how loss of an interferon effector impacts proliferation, cytokine production, and sensitivity to viral infection or chemotherapeutic agents.
Researchers apply this model in antiviral innate immunity studies, particularly to interrogate viral-host interactions in Influenza A, Hepatitis C, or SARS-CoV-2 infection models. The cells are suitable for viral challenge assays, interferon response profiling via ISRE-luciferase reporters, and caspase activity measurements. Further applications include co-immunoprecipitation to map IFIT3-containing complexes, RNA-seq for transcriptomic analysis, and drug screening for compounds that compensate for IFIT3 deficiency. For detailed product information, please contact Ascent Research.
