The CD300LD Knockout T-47D Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the T-47D human breast ductal carcinoma epithelial cell line, designed for loss-of-function studies of the inhibitory immune receptor CD300LD. This heterogeneous pool of gene-disrupted cells, generated without single-cell cloning, captures population-level functional variability and reduces clonal selection artifacts, making it suitable for robust and reproducible investigation of CD300LD-dependent signaling.
The host T-47D cell line was established from the pleural effusion of a 54-year-old female patient with breast ductal carcinoma and serves as a well-characterized hormone-responsive breast cancer model. These cells constitutively express estrogen and progesterone receptors, enabling the study of hormone-driven signaling pathways and their interplay with immune regulatory mechanisms. The epithelial phenotype and molecular features of T-47D render this knockout model highly relevant for translational breast cancer research.
CD300LD is a single-pass type I transmembrane receptor harboring an immunoreceptor tyrosine-based inhibitory motif (ITIM). Upon ligand engagement, including phosphatidylserine and other lipid ligands, the receptor is phosphorylated and recruits SHP-1 and SHP-2 tyrosine phosphatases. These phosphatases dephosphorylate downstream signaling intermediates, leading to suppression of NF-??B and ERK/MAPK pathways. Upstream regulators such as IL-4 and IL-10 cytokines can induce CD300LD expression, integrating it into a broader inhibitory network that modulates leukocyte activation and inflammatory responses.
In the T-47D breast cancer context, CD300LD knockout offers a unique model to investigate how this inhibitory receptor contributes to tumor cell-autonomous behaviors and tumor-immune cell crosstalk. Breast carcinoma cells frequently upregulate immune checkpoints to evade immune surveillance, and CD300LD may represent a novel inhibitory axis. Disruption of CD300LD in these hormone-responsive cells allows detailed analysis of changes in proliferation, migration, apoptosis, and the secretion of inflammatory mediators, as well as altered sensitivity to immune effector mechanisms.
This polyclonal knockout product supports a wide array of assays, including Western blotting and RT-qPCR for confirmation of target disruption, cell proliferation, migration, and apoptosis assays to assess functional consequences, and co-culture systems with immune cells to evaluate tumor-immune interactions. Phospho-signaling analyses can map alterations in SHP-1, SHP-2, NF-??B, and ERK activity. The model is also amenable to drug screening for modulators of CD300LD signaling. For technical support, please contact Ascent Research.
