The MR1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Raji B lymphoblastoid cell line, featuring targeted disruption of the MR1 (major histocompatibility complex class I-related) gene. This product provides a heterogeneous pool of MR1-knockout Raji cells, enabling robust loss-of-function studies without monoclonal selection. The polyclonal format preserves genetic diversity and mitigates clonal artifacts, making it suitable for functional screening and bulk immune-based assays.
The parental Raji cell line is an EBV-positive Burkitt lymphoma-derived B lymphoblastoid line originally isolated from an African male. Raji cells display stable B cell characteristics, including surface expression of antigen-presenting molecules such as MHC class I and the non-classical MHC molecule MR1, as well as constitutive activation of NF-??B signaling. These features make Raji a widely employed model for investigating B cell biology, antigen presentation, and immune surveillance, particularly in the context of innate-like T cell interactions.
MR1 functions as a monomorphic antigen-presenting molecule that loads and presents vitamin B metabolites, including riboflavin-derived 5-OP-RU, to the T cell receptor (TCR) of mucosal-associated invariant T (MAIT) cells. MR1 surface expression depends on association with beta-2 microglobulin (B2M) and is upregulated by pro-inflammatory stimuli such as IFN-?? and TLR agonists through NF-??B signaling. Upon engagement of MR1?Cligand complexes, MAIT cells are activated, leading to downstream signaling events involving ZAP-70, LAT, and NFAT, which drive production of Th1 cytokines (IFN-??, TNF-??) and release of cytotoxic mediators like perforin and granzyme. Thus, MR1 serves as a critical bridge between microbial metabolite sensing and innate antimicrobial immunity.
In the Raji B cell context, MR1-mediated presentation is central to triggering MAIT cell responses against pathogens and tumor cells. Disruption of MR1 expression in this polyclonal knockout population eliminates the surface MR1?CB2M complex, abrogating presentation of riboflavin metabolites. This loss-of-function model is particularly valuable for dissecting MR1-dependent immune recognition pathways in scenarios where B cells act as accessory cells, such as in mucosal immunity or tumor microenvironment interactions. The model allows researchers to separate MR1-specific effects from other antigen presentation routes like classical MHC class I and II pathways.
Research applications include mechanistic studies of MR1-mediated MAIT cell activation, host-pathogen interaction modeling (e.g., Mycobacterium tuberculosis infection), cancer immune evasion studies where MR1 downregulation may escape MAIT cell surveillance, and validation of MR1 as an immunotherapeutic target. Representative assays feature flow cytometry for MR1 and B2M surface staining, co-culture of knockout Raji cells with MAIT cells followed by IFN-?? ELISA, RT-qPCR for MR1 transcript quantification, immunofluorescence microscopy, and MAIT cell-mediated cytotoxicity assays. For further technical specifications or to customize this product for your experimental system, please contact Ascent Research.
