The DMD Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Jurkat T lymphocytes with disrupted dystrophin expression. This polyclonal knockout model retains genetic heterogeneity and provides a loss-of-function tool for studying dystrophin in a human immune cell background. It facilitates investigation of dystrophin??s roles in T lymphocyte adhesion, migration, and immune synapse formation beyond its canonical muscle functions.
Jurkat is an immortalized human T lymphocyte line from acute T cell leukemia, widely used to model T cell receptor signaling and activation. These cells express essential components of the immunological synapse and are amenable to genetic manipulation. Their robust culture characteristics support high-throughput assays, making them a practical host for exploring non-muscle dystrophin functions in adaptive immunity.
Dystrophin, encoded by DMD, bridges the actin cytoskeleton and extracellular matrix through the dystrophin-glycoprotein complex (DGC). It interacts with F-actin, ??-dystroglycan, syntrophins (??/??), dystrobrevin, and sarcoglycans, anchoring laminin-211. In T cells, dystrophin participates in membrane integrity, integrin-mediated adhesion, and NF-??B signaling, with downstream effectors such as nNOS. Transcriptional regulators include MEF2 and MyoD, though immune-specific regulation remains under study. Disruption of DMD abolishes DGC assembly, impairing these pathways.
DMD elimination in Jurkat cells models immune dysfunction associated with Duchenne and Becker muscular dystrophies. Loss of dystrophin may compromise immunological synapse stability, alter calcium responses, and reduce cell adhesion, reflecting patient immune defects. This model enables dissection of dystrophin??s contribution to T cell signaling, particularly NF-??B pathway modulation, and supports research into immunopathogenic mechanisms of dystrophinopathies.
Applications include western blot and immunofluorescence to verify dystrophin knockout, RT-qPCR for transcript analysis, and functional assays such as Transwell migration and matrix adhesion tests. Flow cytometry detects T cell activation markers (CD69, CD25) and calcium flux. Phospho-signaling analysis and drug screening for DGC restoration further exploit this model. For technical inquiries, contact Ascent Research.
