The BTN1A1 Knockout Ca Ski Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell pool derived from Ca Ski human cervical carcinoma cells. This heterogeneous population carries targeted BTN1A1 gene disruptions introduced by CRISPR/Cas9 genome editing, providing a loss-of-function model for studying butyrophilin-mediated immune regulation. The polyclonal format reflects a mixture of edited alleles without clonal isolation, suitable for population-level analyses.
The parental Ca Ski cell line is derived from a cervical epidermoid carcinoma metastasis and harbors integrated HPV-16 genomes. As an epithelial model, it is extensively employed in cancer biology and virology research to study HPV-mediated transformation and immune evasion. These cells respond to inflammatory cytokines, providing a relevant system to assess how viral oncoproteins intersect with host immunomodulatory pathways.
BTN1A1 is a butyrophilin family immune checkpoint protein that inhibits T cell activation by downregulating NF-??B and MAPK signaling downstream of the T cell receptor (TCR). It is induced by inflammatory cytokines (IFN-??, TNF-??) and prolactin, acting through STAT5 and NF-??B transcription factors. BTN1A1 interacts with CD28 and CTLA-4, and forms complexes with xanthine oxidoreductase (XDH) and perilipin-2 (PLIN2). Its signaling attenuates T cell proliferation, alters cytokine profiles, and modulates PI3K-AKT and STAT1/3 pathways, thereby integrating multiple immune regulatory inputs.
In Ca Ski cells, BTN1A1 knockout is predicted to relieve T cell inhibition, potentially enhancing immune recognition of HPV-positive cervical carcinoma. Disruption of this checkpoint may counteract tumor immune evasion strategies exploited by viral oncoproteins, promoting pro-inflammatory responses. The polyclonal population captures heterogeneous editing outcomes, enabling study of variable immune escape mechanisms and facilitating assessment of functional diversity within a cancer cell population.
This knockout model supports diverse assays, including T cell coculture for proliferation and cytokine secretion, flow cytometry for immune checkpoint analysis, and NF-??B reporter measurements. Transcriptomic profiling via RNA-seq can reveal pathway alterations, while migration and invasion assays probe metastatic behavior. These cells are also suitable for drug screening of butyrophilin-targeted immunotherapies. For further details, contact Ascent Research.
