The IRF3 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for functional studies of interferon regulatory factor 3 (IRF3). This product comprises a heterogeneous pool of Jurkat cells carrying targeted disruption of the IRF3 gene, ensuring a robust loss-of-function model without clonal isolation. The polyclonal format helps mitigate potential clonal artifacts and provides a representation of diverse editing outcomes suitable for population-level assays.
The parental Jurkat cell line is an immortalized human T lymphocyte line originally established from the peripheral blood of an acute T cell leukemia patient. These suspension lymphoblastoid cells are widely employed to investigate T cell receptor signaling, cytokine production, and lymphocyte function. The Jurkat background offers a convenient and well-characterized model system for dissecting signaling networks in a T cell context.
IRF3 serves as a pivotal transcription factor in innate immune responses, particularly mediating the induction of type I interferons (IFNs) following viral infection. In the canonical pathway, cytosolic nucleic acid sensors such as RIG-I and MDA5, or the cGAS-STING axis, activate the adaptor proteins MAVS or STING, respectively. This leads to the activation of the kinases TBK1 and IKK??, which phosphorylate IRF3 at C-terminal serine residues. Phosphorylated IRF3 dimerizes and translocates to the nucleus, where it associates with coactivators CBP/p300 and partners such as IRF7 and NF-??B to drive transcription of antiviral genes including IFNB1, ISG15, CXCL10, and OAS1. IRF3 is also engaged downstream of TLR3 and TLR4 through the TRIF adaptor. Thus, IRF3 operates at the convergence of multiple pattern recognition receptor pathways.
In Jurkat T lymphocytes, IRF3 knockout abrogates the type I interferon response, enabling precise dissection of innate immune signaling within a T cell environment. This model is particularly valuable given the emerging roles of T cell-intrinsic innate immune pathways in antiviral immunity, antitumor responses, and autoimmunity. Since Jurkat cells originate from a leukemic T cell lineage, the knockout system also offers a platform to explore the intersection of IRF3 signaling and T cell leukemia biology, where dysregulation of interferon pathways may influence malignant transformation or therapy responses.
Typical research applications include interrogation of the RIG-I/MDA5/MAVS and cGAS/STING/TBK1 signaling axes, antiviral response profiling using viral infection assays, and interferon induction studies via ISRE luciferase reporter assays or quantitative RT-qPCR of downstream targets such as IFNB1 and CXCL10. The polyclonal knockout cells are compatible with flow cytometry, western blotting, ELISA, and RNA-seq for comprehensive pathway analysis. They also support T cell functional studies where intrinsic innate signaling impacts proliferation, activation, or cytokine secretion. For additional information, please contact Ascent Research.
