The CD46 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa cell line, featuring targeted disruption of the CD46 gene. This heterogeneous polyclonal pool serves as a loss-of-function model for investigating the membrane cofactor protein (CD46/MCP) in complement regulation, viral entry, and immune signaling within a human epithelial cell system.
HeLa cells are an HPV18-positive human cervical adenocarcinoma epithelial line extensively employed in biomedical research. Their well-characterized growth properties and epithelial origin make them a robust platform for studying CD46-mediated processes such as pathogen adhesion, complement defense, and immune modulation in a cancer-relevant context.
CD46 encodes a membrane-bound complement regulatory protein that serves as a cofactor for Factor I-mediated inactivation of C3b and C4b, shielding host cells from autologous lysis. Beyond complement regulation, CD46 acts as a receptor for measles virus hemagglutinin, adenovirus fiber, and Neisseria Opa proteins, mediating pathogen entry. In T cells, CD46 ligation provides costimulatory signals that drive IL-10 secretion, modulating adaptive immunity. CD46 transcription is upregulated by inflammatory cytokines IL-1?? and TNF-??, as well as NF-??B, and is modulated by complement activation fragments. Key interacting partners include C3b, C4b, Factor I, viral attachment proteins, and integrin ??v??3. CD46 disruption thus impairs complement defense, enhances C3b/C4b deposition, alters IL-10 production, and blocks specific viral entry mechanisms.
In the HeLa adenocarcinoma background, endogenous CD46 expression ensures that knockout-induced phenotypes faithfully mirror epithelial cell biology. This model reveals roles of CD46 in complement sensitivity, pathogen entry, and immune modulation. Loss of CD46 sensitizes cells to complement-mediated lysis, offering a tool for atypical hemolytic uremic syndrome and autoimmune disease research (e.g., systemic lupus erythematosus). Simultaneously, reduced viral receptor availability permits dissection of measles virus and adenovirus infection pathways, while altered T-cell costimulation and IL-10 release enables cancer immunology studies.
These polyclonal knockout cells are suitable for complement deposition assays (C3b/C4b), viral entry assays, T-cell co-cultures with IL-10 ELISA, and hemolytic complement assays. Western blotting, flow cytometry, apoptosis and migration/invasion assays characterize phenotypic changes. Applications include complement biology, viral pathogenesis, T-cell immunology, drug screening, and disease modeling for atypical HUS. For technical support, please contact Ascent Research.
