For research use only
| Cat No. | ABC-KH003Y |
| Product Type | Knockout Stable Cell Line |
| Cell Type | Monocyte |
| Species | Human |
| Host Cell | THP-1 |
| Source Organ | Peripheral Blood |
| Disease | Acute Monocytic Leukemia |
| Storage | Liquid Nitrogen |
B2M/CIITA Double Knockout THP-1 Cell Line creates an MHC I/II-deficient human macrophage model for advanced immunotherapy and immune evasion research.
B2M/CIITA Double Knockout THP-1 Cell Line is generated from the human monocytic THP-1 cell line using CRISPR/Cas9-mediated gene editing to disrupt both Beta-2-microglobulin (B2M) and Class II Major Histocompatibility Complex Transactivator (CIITA) genes. This dual knockout model exhibits loss of MHC class I (due to B2M knockout) and MHC class II (due to CIITA knockout) expression, making it an ideal tool for studying immune evasion, allogeneic cell therapies, and graft rejection mechanisms. THP-1 cells grow in suspension with round morphology and are widely used in macrophage differentiation, antigen presentation, and immunotherapy research. The edited cells are maintained at low passage numbers (<P20) to ensure genetic stability, with knockout efficiency validated through PCR, sequencing, or Western blot. The cell line undergoes rigorous quality control and is confirmed free of contamination from HIV-1, HBV, HCV, Syphilis, mycoplasma, fungi, yeast, and bacteria.
| Species | Human |
| Cat.No | ABC-KH003Y |
| Product Category | Transfected Stable Cell Lines |
| Size/Quantity | 1 vial |
| Cell Type | Monocyte |
| Growth Mode | Suspension |
| Shipping Info | Dry Ice |
| Growth Conditions | 37 ℃, 5% CO2 |
| Source Organ | Peripheral Blood |
| Disease | Acute Monocytic Leukemia |
| Biosafety Level | 1 |
| Storage | Liquid Nitrogen |
| Product Type | Knockout Stable Cell Line |
| Host Cell | THP-1 |
| Gene Info | B2M / CIITA |
| Quality Control | All cells test negative for mycoplasma, bacteria, yeast, and fungi. |
The B2M/CIITA Double Knockout THP-1 Cell Line is a genetically engineered human monocytic model featuring concurrent disruption of both β2-microglobulin (B2M) and MHC class II transactivator (CIITA) genes, resulting in complete deficiency of MHC class I and class II surface expression. This dual modification creates a powerful experimental system for studying immune evasion mechanisms, NK/T cell interactions, and MHC-independent immune responses. The cell line retains THP-1’s differentiation capacity while providing a unique platform for investigating tumor immunology, allogeneic cell therapies, and fundamental antigen presentation processes.