Human CD47 Knockout Cell Line-Jurkat
Cat.No. : CSC-RT2699
Host Cell: Jurkat Target Gene: CD47
Size: 1x10^6 cells/vial, 1mL Validation: Sequencing
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Cell Line Information
Cell Culture Information
Safety and Packaging
| Cat. No. | CSC-RT2699 |
| Cell Line Information | This cell is a stable cell line with a homozygous knockout of human CD47 using CRISPR/Cas9. |
| Target Gene | CD47 |
| Host Cell | Jurkat |
| Size Form | 1 vial (10^6 cell/vial) |
| Shipping | Dry ice package |
| Storage | Liquid nirtogen |
| Species | Human |
| Revival | Rapidly thaw cells in a 37°C water bath. Transfer contents into a tube containing pre-warmed media. Centrifuge cells and seed into a 25 cm2 flask containing pre-warmed media. |
| Mycoplasma | Negative |
| Format | One frozen vial containing millions of cells |
| Storage | Liquid nitrogen |
| Safety Considerations |
The following safety precautions should be observed. 1. Use pipette aids to prevent ingestion and keep aerosols down to a minimum. 2. No eating, drinking or smoking while handling the stable line. 3. Wash hands after handling the stable line and before leaving the lab. 4. Decontaminate work surface with disinfectant or 70% ethanol before and after working with stable cells. 5. All waste should be considered hazardous. 6. Dispose of all liquid waste after each experiment and treat with bleach. |
| Ship | Dry ice |
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Background
Case Study
Applications
CD47 is an immunoglobulin that is overexpressed on the surface of many cancer cells. CD47 forms a signaling complex with signal regulatory protein alpha (SIRPα), which promotes cancer cells to escape from macrophage-mediated phagocytosis. In recent years, CD47 has been shown to be highly expressed in many types of solid tumors and is associated with poor patient prognosis. More and more studies have shown that inhibiting the CD47-SIRPα signaling pathway can promote adaptive immune responses and enhance the phagocytosis of tumor cells by macrophages.
CD47 on the surface of tumor cells inhibits the phagocytosis of macrophages by interacting with signal regulatory protein alpha (SIRPα) on the surface of macrophages. The mechanism is that after SIRPα interacts with CD47, it promotes the localization of SIRPα to the phagocytic synapse, activates Src homology region 2 domain phosphatase-1, and finally inhibits the accumulation of non-myosin IIA on the cell membrane, preventing tumor cells from being phagocytosed. Many studies have promoted the phagocytosis of tumor cells by macrophages by blocking the CD47-SIRPα signaling pathway, thereby achieving the purpose of treating tumors. Preclinical and clinical studies have used a variety of CD47-targeted antibodies to treat tumors and achieved good therapeutic effects, providing convincing evidence for the therapeutic potential of targeting the CD47-SIRPα axis in tumors.
CD47 is a ubiquitously expressed cell surface glycoprotein that has been implicated in immune evasion. It interacts with the inhibitory receptor signal regulatory protein α (SIRPα), which is primarily expressed on myeloid cells and normally functions to limit effector functions such as phagocytosis and immune cell homeostasis. CD47/SIRPα antagonists, often referred to as "macrophage checkpoint" inhibitors, are being developed as cancer interventions. SRF231 is an investigational fully human IgG4 anti-CD47 antibody currently being evaluated in clinical trials. The studies here demonstrate that SRF231 binds CD47 and disrupts the CD47/SIRPα interaction without causing hemagglutination or erythrophagocytosis. SRF231 exerts antitumor activity in vitro through phagocytosis and cell death in a manner that is dependent on activation of the Fc-gamma receptor (FcγR) CD32a. Through its Fc domain, SRF231 binds to macrophage-derived CD32a and plays a dual role, initiating FcγR-mediated phagocytosis of cancer cells and acting as a scaffold to drive CD47-mediated death signals into tumor cells.
In this study, SRF231 specifically bound to CD47, as shown by surface staining of WT Jurkat cells expressing CD47, but not to CD47 knockout Jurkat cells (Figure 1A). Multiple human tumor cell lines of the hematopoietic lineage were sensitive to SRF231-mediated phagocytosis by primary human macrophages (Figure 1B). In addition, a significant enhancement of phagocytosis of primary AML bone marrow cells was observed in the presence of SRF231 (Figure 1C). As expected, SRF231 synergized with anti-CD20 antibodies, resulting in enhanced antibody-dependent cellular phagocytosis (ADCP) of the malignant B-cell lymphoma cell lines Raji and SU-DHL-4 (Figure 1D).
Figure 1. SRF231 binds to human CD47 and induces phagocytosis of tumor cells in vitro. (Peluso M O, et al., 2020)
Applications of Human CD47 Knockout Cell Line-Jurkat
1. Immuno-oncology Research: The Human CD47 Knockout (KO) Cell Line-Jurkat is extensively used in immuno-oncology studies to understand the role of CD47 in cancer immune evasion. CD47, known as the “don’t eat me” signal, interacts with signal regulatory protein-alpha (SIRPα) on macrophages to inhibit phagocytosis. Utilizing CD47 KO cells helps elucidate how the loss of this interaction impacts tumor-cell recognition and destruction by the immune system, providing critical insights into the development of CD47-targeted therapies.
2. Drug Development and Therapeutic Targeting: This cell line serves as a valuable tool for testing CD47-targeting monoclonal antibodies (mAbs) and other therapeutic agents. By comparing the responses between wild-type and CD47 KO Jurkat cells, researchers can effectively assess the efficacy and specificity of potential drugs aimed at blocking CD47 to promote cancer cell clearance.
3. Signal Transduction Pathways: Human CD47 KO Cell Line-Jurkat is utilized to investigate signaling pathways involved in cell survival, apoptosis, and immune modulation. The absence of CD47 allows scientists to delineate its role and the downstream effects of its signaling, thereby uncovering new targets for therapeutic intervention.
4. Hematologic Disorders: Since Jurkat is a human T-cell leukemia cell line, CD47 KO variants are especially relevant in studying hematologic malignancies. Researchers leverage this model to understand the mechanisms driving leukemia and lymphoma, aiming to identify novel therapeutic strategies that can overcome resistance and improve patient outcomes.
5. Research in Autoimmune Diseases: CD47 has been implicated in various autoimmune diseases. The Jurkat CD47 KO cell line aids in unraveling the role of CD47 in immune regulation and tolerance. Understanding how CD47 influences autoimmunity can lead to potential therapeutic approaches for conditions such as rheumatoid arthritis and multiple sclerosis.
For research use only. Not intended for any clinical use.
