The ITGB2 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from Jurkat T cells, harboring targeted disruption of the ITGB2 gene. This loss-of-function model is generated by CRISPR/Cas9-mediated gene editing, yielding a heterogeneous pool of cells with ITGB2 inactivation, suitable for studying integrin-dependent processes without clonal selection biases.
Jurkat cells are an immortalized human T lymphocyte line from a T cell leukemia patient, extensively used to model T cell signaling, activation, and immune synapse formation. Their well-characterized pathways and robust growth make them ideal for examining integrin biology; they endogenously express LFA-1 (??L??2 integrin), which relies on the ITGB2-encoded CD18 subunit for adhesion and costimulation.
ITGB2 encodes CD18, the common ??2 subunit of leukocyte integrins, which forms heterodimers with CD11a (ITGAL), CD11b (ITGAM), or CD11c (ITGAX). Integrin activation is triggered by inside-out signals from the T cell receptor and chemokine receptors, requiring the adaptors Talin and Kindlin-3 to induce high-affinity ligand binding. Upon engaging ICAM-1 or ICAM-2, these integrins transmit outside-in signals via FAK and Src kinases, leading to activation of small GTPases RhoA and Rac1, and downstream pathways including NF-??B, ERK, and JNK, which orchestrate cytoskeletal dynamics and transcriptional responses.
In Jurkat cells, ITGB2-dependent LFA-1 function is critical for stable adhesion to ICAM-1, immune synapse formation, and T cell costimulation. Knockout of ITGB2 abolishes these processes, resulting in impaired conjugate formation, reduced IL-2 secretion, and defective migratory responses. This model mimics features of Leukocyte Adhesion Deficiency type 1 (LAD1) and serves as a platform to dissect integrin-mediated signaling in autoimmune and inflammatory disorders.
Typical applications include Western blotting and flow cytometry for CD18 loss, ICAM-1 adhesion assays, Transwell migration assays, T cell activation measurements (e.g., IL-2 secretion, NFAT luciferase reporter), and cell aggregation studies. These assays facilitate research into leukocyte adhesion, T cell costimulation, LAD1 pathology, and high-throughput screening of integrin-targeted drugs. For additional details, please contact Ascent Research.
