The CD200R1L Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population in which the CD200R1L gene has been disrupted, creating a loss-of-function model for studying inhibitory immune receptor signaling. Derived from the near-haploid HAP1 cell line, this population enables functional genomic analyses and facilitates high-throughput screening of modulators targeting the CD200?CCD200R1L axis.
HAP1 cells originate from the KBM-7 chronic myeloid leukemia (CML) cell line and exhibit a near-haploid, adherent fibroblast-like morphology. Their haploid karyotype removes the complexity of diploid genetics, making them an exceptional host for CRISPR/Cas9 knockout experiments. These cells maintain key myeloid and signaling pathways, offering a biologically relevant platform to investigate immune checkpoint receptors and their downstream effectors.
CD200R1L is an inhibitory receptor belonging to the CD200 receptor family, characterized by cytoplasmic ITIM motifs. Ligand engagement by CD200 triggers recruitment of the phosphatases SHP-1 and SHP-2, which dephosphorylate intermediates in the MAPK and NF-??B cascades, leading to attenuation of pro-inflammatory responses in myeloid cells. This signaling loop serves as a critical immune checkpoint that maintains tolerance and prevents overactivation.
CD200R1L knockout in the HAP1 near-haploid background allows unambiguous assessment of receptor function without interference from a second allele. The model enables precise characterization of CD200-dependent inhibitory signaling, including measurement of SHP-1/SHP-2 activation and downstream kinase activity. Its relevance extends to disease models of chronic inflammation, autoimmunity, and tumor immune escape, where CD200R1L-mediated immunosuppression plays a pathogenic role.
These polyclonal knockout cells are applicable to a wide range of assays, such as flow cytometry for receptor surface expression, CD200 binding studies, phospho-SHP Western blotting, and multiplex cytokine secretion ELISA. Using this system, researchers can dissect the molecular mechanisms of immune checkpoint regulation and screen for therapeutic candidates that block or enhance CD200R1L signaling. For additional product details and technical support, contact Ascent Research.
