The KLRB1 knockout TE1 polyclonal cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human esophageal squamous cell carcinoma line TE1. These cells harbor a targeted disruption of the KLRB1 gene, which encodes the C-type lectin receptor CD161, a key regulator of NK and T cell cytotoxicity and cytokine production. The polyclonal format provides a heterogeneous mixture of edited alleles, enabling robust loss-of-function studies without clonal selection. This product is intended for researchers investigating CD161-mediated signaling pathways in cancer biology and tumor-immune interactions.
The TE1 host cell line is a well-differentiated human esophageal squamous cell carcinoma line widely employed in esophageal cancer research. It serves as a representative model for studying tumor cell-intrinsic signaling, immune evasion mechanisms, and responses to therapeutic interventions. The well-characterized background of TE1 cells allows for reproducible and physiologically relevant experiments, making it a suitable platform for dissecting the functions of immune-modulatory genes such as KLRB1.
KLRB1 encodes CD161, an inhibitory C-type lectin receptor expressed on NK cells and T cells. Upon ligand LLT1 (CLEC2D) engagement, CD161 recruits the phosphatase SHP-1 via cytoplasmic ITIM motifs, leading to dephosphorylation of downstream signaling molecules and attenuation of immune responses. This pathway negatively regulates NK cell degranulation, evidenced by reduced perforin and granzyme B release, and suppresses IFN-?? production. The expression and activity of KLRB1 are modulated by upstream cytokines IL-2, IL-12, and IL-15. In the context of cancer, CD161 signaling is thought to dampen antitumor immunity, thereby promoting immune evasion.
Introduction of a CRISPR/Cas9-mediated KLRB1 knockout in TE1 cells eliminates CD161 expression and disrupts the LLT1?CSHP-1?CITIM signaling axis, providing a unique model to dissect how esophageal squamous carcinoma cells regulate immune recognition. By abrogating KLRB1 function, researchers can directly evaluate changes in cytokine secretion profiles, susceptibility to NK and T cell-mediated cytotoxicity, and global transcriptional alterations. This model is especially valuable for exploring the crosstalk between tumor-intrinsic pathways and the local immune microenvironment, offering insights into potential immune escape mechanisms in esophageal cancer.
The KLRB1 knockout TE1 polyclonal cells support a broad range of experimental applications, including co-culture cytotoxicity assays with primary NK cells or T cell lines to quantify tumor cell lysis, flow cytometric analysis of CD161 expression, Western blotting and RT-qPCR for detecting signaling mediators such as SHP-1 and IFN-??, and ELISA-based measurement of secreted cytokines. Transcriptomic profiling by RNA-seq can uncover global gene expression changes associated with KLRB1 loss, while Sanger sequencing can verify the editing outcomes within the heterogeneous population. These capabilities enable drug target validation and functional screening of immunomodulatory compounds targeting the KLRB1 pathway. For further information, please contact Ascent Research.
