The KLRB1 Knockout T-47D Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the T-47D human breast cancer cell line, designed for targeted disruption of the KLRB1 gene. This product provides a heterogeneous knockout model that preserves genetic diversity, enabling population-level studies of gene function. KLRB1 encodes CD161, an inhibitory C-type lectin receptor, and its disruption facilitates investigation of immune-regulatory mechanisms in a luminal A breast cancer context.
The T-47D cell line originates from the pleural effusion of a ductal carcinoma patient and is widely used as a model of hormone-responsive, luminal A breast cancer. These cells express estrogen and progesterone receptors, making them ideal for studying endocrine-dependent tumor biology and the interplay between epithelial cancer cells and the immune microenvironment. The metastatic origin of T-47D adds clinical relevance for examining genes involved in tumor progression and immune evasion.
CD161 functions as an inhibitory receptor that, upon binding to CLEC2D (LLT1), recruits SHP-1 and SHP-2 phosphatases via its ITIM domain, dampening lymphocyte activation. Upstream cytokines IL-12, IL-15, and IL-18 regulate KLRB1 expression, while downstream signaling leads to reduced IFN-?? secretion and attenuated cytotoxicity. This pathway is central to NK and T cell regulation, with implications for tumor immune surveillance.
In the T-47D model, KLRB1 knockout allows dissection of CD161-mediated immune checkpoint functions within the breast cancer microenvironment. Loss of CD161 may alter tumor-immune cell interactions, affecting NK cell-mediated cytotoxicity and cytokine responses. This system is valuable for exploring mechanisms of immune evasion and potential therapeutic interventions in luminal A breast cancer, where immune contexture impacts patient outcomes.
This polyclonal knockout model supports diverse applications, including cancer immunotherapy target validation, NK cell biology studies, and breast cancer immune microenvironment research. Researchers can assess knockout efficiency by NGS analysis, quantify gene expression by RT-qPCR and Western blotting, and evaluate functional responses using co-culture cytotoxicity assays and cytokine ELISA. Flow cytometry and phospho-signaling analysis further enable characterization of immune signaling changes. For more information, contact Ascent Research.
