The CD46 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from human Raji B lymphocytes, with disrupted CD46 expression. This polyclonal format provides a heterogeneous pool of gene-edited cells, avoiding clonal selection and offering a loss-of-function model that retains population-level genetic diversity. It is designed for studying CD46??s roles in complement regulation, viral pathogenesis, and immune modulation without the constraints of monoclonality.
Raji is an EBV-positive Burkitt lymphoma B-cell line widely used in immunology and oncology. It expresses surface complement receptors and MHC molecules, making it a relevant model for B-cell signaling, antigen presentation, and viral interactions. The cells grow rapidly in suspension, facilitating large-scale experiments, and their cancerous B-cell context is ideal for investigating complement evasion mechanisms and viral entry pathways.
CD46 is a membrane glycoprotein that serves as a cofactor for factor I-mediated cleavage of C3b and C4b, thereby inhibiting MAC formation and protecting cells from complement lysis. It also functions as a receptor for measles virus hemagglutinin and adenovirus fiber protein. On T cells, CD46 engagement can provide costimulatory signals and, through SPAK/JNK signaling, promote regulatory T-cell differentiation and IL-10 production. Its expression is upregulated by TNF-?? and IFN-??, and it interacts with C3b, C4b, factor I, and tetraspanins CD9/CD81, linking complement regulation to adaptive immunity.
In Raji cells, CD46 knockout abrogates complement protection, rendering these B lymphoma cells susceptible to complement-mediated lysis and enabling detailed study of immune evasion. The loss of CD46 also abolishes measles virus entry, providing a defined system for viral attachment and tropism research. The polyclonal nature mirrors the heterogeneity found in tumors, making this model suitable for preclinical assessment of CD46-targeted therapies and for exploring the interplay between complement and viral oncogenesis in EBV-related cancers.
Key applications include complement lysis assays to quantify CD46-dependent protection, flow cytometric measurement of CD46 expression and viral binding, Western blotting for protein validation, and co-culture experiments to assess T-cell costimulation. The cells are also useful for high-content screening of complement-modulating compounds or viral entry inhibitors. For further information or technical support, please contact Ascent Research.
