The CD46 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat human T lymphocyte cell line, engineered to disrupt the CD46 gene. This pool of genetically heterogenous cells provides a loss-of-function model for studying CD46-dependent processes without the need for clonal selection. The population-level gene disruption facilitates robust and reproducible analysis of CD46 function in T cell biology, complement regulation, and pathogen entry.
Jurkat cells are a well-established human T lymphocyte line originally isolated from a patient with acute lymphoblastic leukemia. They serve as a model system for investigating T cell signaling, activation, and leukemia biology. The Jurkat line constitutively exhibits many characteristics of mature T cells, including surface expression of the T cell receptor (TCR) and associated signaling machinery, making it suitable for probing CD46 co-stimulatory and regulatory functions.
CD46, also known as membrane cofactor protein (MCP), is a type I transmembrane glycoprotein that functions as a key regulator of complement activation. It binds complement components C3b and C4b and serves as a cofactor for the serine protease complement factor I, facilitating the proteolytic cleavage and inactivation of C3b and C4b, thereby protecting host cells from autologous complement attack. Beyond complement regulation, CD46 acts as a co-stimulatory molecule in T cells, where its ligation can modulate differentiation and cytokine secretion. Signaling through CD46 involves activation of Vav1 and ERK1/2, leading to downstream events such as IL-10 secretion and autophagy induction. Additionally, CD46 is exploited as a cellular receptor by several pathogens: the measles virus hemagglutinin protein and adenovirus fiber protein bind CD46 to mediate viral entry. CD46 also interacts with integrin ??1, CD9, and CD81, forming molecular complexes that influence adhesion and signaling.
In Jurkat T cells, disruption of CD46 abrogates its complement regulatory activity, rendering the cells susceptible to complement-mediated lysis in experimental settings. Moreover, loss of CD46 expression eliminates its co-stimulatory input, which can alter T cell receptor-driven responses, including phosphorylation of Vav1 and ERK, and reduce IL-10 production, thereby affecting the balance of T helper cell differentiation. The absence of CD46 also impedes measles virus and adenovirus entry, making this knockout population a valuable tool for dissecting viral infection mechanisms in a lymphocytic background. This model thus allows for precise interrogation of CD46-dependent pathways in a context that combines complement biology with adaptive immunity.
Researchers can employ these CD46 knockout polyclonal Jurkat cells in a variety of assays, including flow cytometric verification of CD46 loss, complement-dependent cytotoxicity assays, measles virus or adenovirus entry experiments, and ELISA for IL-10 secretion. Western blotting can assess downstream signaling molecules such as phosphorylated Vav1 and ERK, while RT-qPCR enables quantitative analysis of cytokine and effector gene expression. These cells are ideal for drug screening in complement regulation, viral entry inhibition, or T cell co-stimulation modulation. For further information or to order this product, please contact Ascent Research.
