The CD47 Knockout Raji Polyclonal Cells provide a genetically disrupted polyclonal population of Raji B-lymphocyte cells, generated by CRISPR/Cas9-mediated targeting of the CD47 gene. This product is supplied as a pool of edited cells, eliminating the inhibitory CD47 ligand without clonal selection, thereby preserving heterogeneous knockout profiles suitable for population-based functional studies.
The Raji host cell line is a suspension-adapted, Epstein-Barr virus (EBV)-positive lymphoblastoid line derived from a pediatric Burkitt lymphoma patient. Raji cells exhibit characteristic B-cell surface markers including CD19, CD20, CD22, and surface IgM, and they serve as a widely used model for B-cell lymphoma biology, immune cell interactions, and oncogenic signaling.
CD47 encodes a multifunctional cell surface glycoprotein that functions as a pivotal immune checkpoint molecule. Through engagement of signal-regulatory protein alpha (SIRP??) on macrophages, CD47 recruits SHP-1 and SHP-2 phosphatases to transduce an anti-phagocytic ‘don’t eat me’ signal. CD47 also interacts with thrombospondin-1 and integrins ??v??3 and ??IIb??3 to modulate cell adhesion, migration, and apoptosis, activating downstream effectors including FYN, FAK, and Rho GTPases. Transcriptionally, CD47 is regulated by HIF-1??, MYC, and NF-??B in response to cytokines such as TNF-?? and hypoxic stress, integrating signals that control immune evasion, vascular remodeling, and cell survival.
In the Raji background, CD47 disruption abrogates the dominant inhibitory interaction with macrophage SIRP??, thereby promoting phagocytic clearance of lymphoma cells. This knockout model replicates a critical axis of tumor immune escape and enables dissection of CD47-SIRP?? checkpoint blockade in a relevant B-cell malignancy context. The EBV-driven lymphoblastoid phenotype further allows investigation of CD47-dependent innate immune regulation in virally transformed cells.
Researchers can employ these cells in a range of immunotherapeutic and functional assays, including macrophage co-culture phagocytosis assays (ADCP), antibody-dependent cellular phagocytosis reporter systems, flow cytometric confirmation of CD47 loss, co-immunoprecipitation of CD47-SIRP?? interactions, and cell adhesion or migration studies. The polyclonal knockout population is especially suited for screening therapeutic antibodies, evaluating immune checkpoint inhibitors, and probing signal transduction pathways downstream of CD47. For detailed technical specifications and support, contact Ascent Research.
