The B2M Knockout KYSE-150 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human esophageal squamous cell carcinoma line KYSE-150, engineered to disrupt the B2M gene encoding beta-2-microglobulin. This genetically heterogeneous pool of cells models loss-of-function of B2M, enabling robust investigation of MHC class I-dependent antigen presentation without assuming clonal uniformity or specific editing outcomes. The polyclonal format captures the diversity of gene-disrupted alleles across the population, closely mimicking tumor heterogeneity and providing a versatile tool for functional genomics and immune-oncology studies.
The host cell line KYSE-150 originates from a poorly differentiated human esophageal squamous cell carcinoma, a disease model characterized by aggressive growth and clinically relevant immune evasion features. Its genetic background retains many hallmarks of esophageal carcinoma, including dysregulated signaling and altered antigen processing, making it a pertinent system for evaluating immune recognition mechanisms. The esophageal squamous cell carcinoma origin provides a contextually appropriate environment for studying how beta-2-microglobulin loss influences tumor?Cimmune interactions in a cancer type with high unmet clinical need.
Beta-2-microglobulin, the B2M gene product, functions as an essential chaperone for the assembly and cell surface trafficking of MHC class I heavy chains (HLA-A, B, C). It forms a stable complex with heavy chains, calreticulin, tapasin, the TAP1/TAP2 peptide transporter, and ERp57 within the peptide-loading complex, a process activated by upstream regulators such as interferon gamma (IFN-??) via STAT1 and IRF1, and influenced by NF-??B. Disruption of B2M prevents proper MHC class I folding, thereby blocking surface expression and downstream activation of CD8+ T cells through immune synapse formation. Consequently, this knockout model intercepts the canonical MHC class I antigen processing and presentation pathway, providing a clean loss-of-function phenotype for dissecting mechanisms of adaptive immunity.
In the KYSE-150 esophageal carcinoma context, B2M knockout mirrors a clinically observed immune evasion strategy, where tumors downregulate MHC class I to escape CD8+ T cell-mediated cytotoxicity. This model enables systematic analysis of how esophageal squamous cell carcinoma cells become invisible to the adaptive immune system, supporting studies on tumor escape, immunotherapy resistance, and the identification of synthetic lethal partners that selectively target B2M-deficient cancer cells. The polyclonal nature further permits the evaluation of population-level heterogeneity in antigen presentation capacity and immune recognition.
Typical research applications include flow cytometric quantification of MHC class I surface expression upon IFN-?? stimulation, western blotting for beta-2-microglobulin, and co-culture cytotoxicity assays with antigen-specific CD8+ T lymphocytes to functionally assess immune evasion. Additional uses encompass RNA-seq profiling of transcriptomic changes, immunofluorescence microscopy for MHC class I localization, and CRISPR-based synthetic lethality screens. These polyclonal knockout cells serve as an advanced platform for immunotherapy development, target validation, and mechanistic interrogation of tumor immunology. For further technical specifications or ordering details, please contact Ascent Research.
