The TNFRSF1B Knockout Jurkat E6.1 Cell Line is a CRISPR/Cas9-edited knockout cell line that provides targeted disruption of the TNFRSF1B gene, which encodes tumor necrosis factor receptor 2 (TNFR2). This model enables precise investigation of TNFR2-mediated signaling in a human T lymphocyte background. Generated through CRISPR/Cas9-mediated gene editing, this cell line lacks functional TNFR2 expression and is supplied as a live, growing culture ready for downstream functional assays.
The host cell line, Jurkat E6.1, is an immortalized human T lymphoblastoid line derived from acute T cell leukemia. It is widely utilized as a model system for T cell receptor (TCR) signaling, T cell activation, and immune response studies. Jurkat cells retain key T cell features, including CD3/TCR complex expression and responsiveness to activating stimuli. Their robust proliferation and amenability to genetic manipulation make them an ideal platform for generating gene-edited derivatives such as this knockout line.
TNFRSF1B encodes TNFR2, a receptor that binds both membrane-bound and soluble TNF-??, as well as lymphotoxin-??. Upon ligand engagement, TNFR2 recruits adaptor proteins TRAF2 and TRAF1, along with cIAP1/2, to initiate intracellular signaling cascades. This triggers activation of the non-canonical NF-??B pathway via stabilization of NIK and processing of p100 to p52, as well as canonical NF-??B signaling through RIPK1, TAK1, and the IKK complex. Additionally, TNFR2 stimulates the JNK pathway via ASK1 and engages PI3K-AKT signaling. Key downstream targets include anti-apoptotic genes BCL2L1 and BIRC3, and the cytokine IL2. Disruption of TNFRSF1B in this cell line abrogates these signaling events, impairing NF-??B-driven pro-survival and proliferative programs.
In T lymphocytes, TNFR2 serves as a co-stimulatory receptor that augments TCR-induced signals, enhancing T cell survival and proliferation. Its expression is upregulated upon T cell activation and is critical for regulatory T cell function and immune homeostasis. The Jurkat E6.1 background provides a relevant context to dissect TNFR2-specific contributions, independent of TNFR1 effects. This knockout model facilitates studies on the crosstalk between TNFR2, PI3K-AKT, and JNK pathways, and is valuable for modeling pathological conditions such as autoimmunity and cancer, where dysregulated TNFR2 signaling plays a role.
Researchers can employ this cell line in a range of assays, including Western blotting for NF-??B pathway components (e.g., p100/p52, phospho-p65), flow cytometric apoptosis detection with Annexin V, RT-qPCR analysis of downstream gene expression, cell proliferation assays under TNFR2 stimulation, and phospho-JNK ELISA. The model supports investigations into TNFR2-mediated T cell biology, drug screening for TNFR2-targeted therapies, and studies of immune dysregulation in autoimmune diseases and cancer immunotherapy. For further information or to place an order, please contact Ascent Research.
