The BTN2A1 Knockout Jurkat Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal population with disrupted BTN2A1 gene in the Jurkat T lymphocyte cell line. Unlike monoclonal knockout lines, this heterogeneous pool retains diverse editing outcomes, avoiding clonal selection biases and better representing population-level gene perturbation. The loss-of-function model is generated by CRISPR/Cas9-mediated genomic disruption, enabling researchers to investigate the role of BTN2A1 in immune regulatory pathways with high biological relevance.
Jurkat cells are an immortalized human T lymphocyte line originally established from an acute T cell leukemia patient. They are a cornerstone model for studying T cell signaling, activation, and apoptosis, owing to their robust expression of TCR signaling components. Researchers extensively use Jurkat cells to examine molecular events in T cell responses, including cytokine production, costimulatory signals, and immune checkpoint regulation. This established background ensures reproducible results for functional genomics studies of immunomodulatory genes such as BTN2A1.
BTN2A1 is a member of the butyrophilin family of immune regulatory proteins, critically involved in phosphoantigen sensing by V??9V??2 T cells. It functions by interacting with BTN3A1 to present phosphoantigens to the V??9V??2 TCR, which triggers phosphorylation of ITAM-bearing adaptors, recruitment of Syk and ZAP70 kinases, and subsequent activation of MAPK/NF-??B signaling cascades. This pathway leads to expression of T cell activation markers CD69 and CD25 and the production of effector cytokines. BTN2A1 expression itself is positively regulated by TCR stimulation and cytokines such as IL-2, and the protein can mediate both costimulatory and inhibitory signals depending on context. In the Jurkat cellular context, disruption of BTN2A1 eliminates its contribution to these butyrophilin-dependent regulatory mechanisms, providing a clean loss-of-function model.
By knocking out BTN2A1 in Jurkat T lymphocytes, this polyclonal population becomes an invaluable tool for dissecting ?æ? T cell recognition and butyrophilin-mediated immune regulation. Since Jurkat cells do not express the V??9V??2 TCR endogenously, the model is particularly suited for studying the interplay between butyrophilin family members and the downstream signaling networks that are shared with conventional ???? T cells. Researchers can use these cells to interrogate how BTN2A1 modulates T cell activation thresholds, cytokine production, and signaling crosstalk, shedding light on mechanisms relevant to autoimmune diseases, hematologic malignancies, and immune dysregulation disorders.
This product can be employed in a wide range of assays to study BTN2A1 function and immune cell signaling. Typical applications include flow cytometry to confirm BTN2A1 loss, western blotting and RT-qPCR for expression analysis, phospho-signaling assays for ZAP70 or Syk, co-culture experiments with V??9V??2 T cells to measure cytokine production via ELISA or activation marker upregulation (CD69/CD25), and reporter assays for NF-??B or NFAT activity. The knockout model is also valuable for immune checkpoint biology, phosphoantigen sensing, and development of cancer immunotherapies targeting butyrophilin pathways. For further information or custom applications, contact Ascent Research.
