The IL6ST Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Jurkat cells carrying targeted disruption of the IL6ST gene (gp130). This loss-of-function model enables dissection of IL-6 family cytokine signaling in a T-lymphocyte background. The polyclonal format avoids clonal selection artifacts, providing a heterogeneous knockout representation suitable for pathway analysis.
Jurkat cells, derived from an acute T-cell leukemia patient, are widely used to study T-cell signaling, HIV infection, and immune responses. Their rapid proliferation and genetic tractability make them ideal for knockout studies. IL6ST disruption in this context permits investigation of gp130-dependent functions in T-cell activation, survival, and cytokine-driven processes.
IL6ST encodes gp130, the shared signal-transducing receptor subunit for the IL-6 family of cytokines, including IL-6, IL-11, LIF, oncostatin M, CNTF, and cardiotrophin-1. Upon ligand binding, gp130 dimerizes with a ligand-specific ??-receptor (e.g., IL6R for IL-6) and activates associated JAK kinases (JAK1, JAK2, TYK2), leading to tyrosine phosphorylation of gp130 and recruitment of STAT3 and STAT1. In parallel, the SHP2?CGRB2?CGab1 axis triggers the Ras?CMAPK/ERK and PI3K/Akt pathways. Activated STAT3 induces transcription of target genes such as SOCS3 (a negative regulator), Bcl-xL, Cyclin D1, c-Myc, Mcl-1, and VEGF, thereby promoting cell survival, proliferation, and pro-inflammatory signaling.
Although gp130 is best characterized in non-hematopoietic cells, it is expressed in T lymphocytes and contributes to T-cell activation and differentiation under inflammatory conditions. In Jurkat cells, IL6ST disruption allows clean interrogation of IL-6 family cytokine effects on TCR-mediated signals, apoptosis sensitivity, and cytokine release, including IL-6 trans-signaling. This knockout model is particularly relevant for dissecting STAT3-dependent gene programs in leukemic T cells, studying mechanisms of cytokine release syndrome, and evaluating how gp130 signaling intersects with NFAT or NF-??B pathways.
Applications include monitoring STAT3/ERK1/2 phosphorylation by Western blot after cytokine stimulation, RT-qPCR for SOCS3 and Bcl-xL, flow cytometry for apoptosis/proliferation, co-immunoprecipitation of gp130 complexes, and STAT3-reporter assays. The cells support drug screening for JAK/STAT3 inhibitors and modeling of rheumatoid arthritis or Crohn??s disease pathways. For further technical details, please contact Ascent Research.
