The B2M Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of human 143B osteosarcoma cells with targeted disruption of the B2M gene. This knockout model abolishes beta-2 microglobulin protein production, leading to loss of MHC class I surface expression across the cell pool. The polyclonal format avoids clonal variation while providing a uniform functional knockout, suitable for studies requiring population-level effects.
The 143B cell line is a human osteosarcoma model with a TK-negative phenotype and strong tumorigenicity in nude mice, widely employed for xenograft assays. Its osteoblastic characteristics and robust in vivo growth make it a preferred host for cancer research. Engineering B2M knockout in this background creates a platform to examine MHC class I-dependent immune interactions in bone cancer.
B2M encodes beta-2 microglobulin, which pairs with HLA class I heavy chains to form functional MHC class I molecules. Inside the ER, B2M stabilizes the peptide-loading complex containing TAP1/2, tapasin, calreticulin, and ERp57, enabling peptide binding and surface trafficking. Transcription of B2M is potently activated by IFN-?? and TNF-?? via STAT1, IRF1, and NF-??B pathways. On the cell surface, MHC class I complexes present antigens to CD8+ T cells and engage inhibitory receptors like LILRB1 on NK cells; thus, B2M loss impairs adaptive immunity while sensitizing to innate killing.
Within the 143B osteosarcoma context, B2M knockout generates MHC class I-null tumor cells that evade CD8+ T cell detection but become susceptible to NK cell lysis through missing-self recognition. This mirrors immune evasion tactics in many solid tumors and provides a controlled system to investigate the balance between T cell and NK cell surveillance. The model is particularly relevant for bone cancer, where such immune dynamics influence tumor progression and responses to immunotherapy.
Key applications include flow cytometric analysis of MHC class I loss using pan-HLA antibodies, T cell cytotoxicity co-cultures, and NK cell killing assays to assess missing-self responses. Xenograft studies with knockout cells in immunodeficient or humanized mice enable preclinical testing of checkpoint inhibitors, CAR-T cells, and other immunotherapies. The model also supports mechanistic work on antigen processing machinery and interferon signaling. For further information, please contact Ascent Research.
