The CD1C Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 human cell line, with targeted disruption of the CD1C gene. This loss-of-function model abolishes CD1c protein expression, enabling researchers to investigate CD1c-dependent lipid antigen presentation pathways. As a heterogeneous pool of edited cells, the polyclonal population provides a cost-effective and reproducible tool for functional studies without single-cell cloning. The knockout is generated using CRISPR/Cas9-mediated gene disruption, ensuring efficient ablation of CD1c function across the cell pool.
The HAP1 host cell line is a near-haploid human cell line originally derived from a male patient with chronic myeloid leukemia (CML). These fibroblast-like cells harbor the BCR-ABL1 fusion gene, and their near-haploid karyotype, characterized by a single allele for most genes, simplifies genetic manipulation and analysis. HAP1 cells are widely employed in functional genomics and cancer biology research due to their robust growth and ease of CRISPR-based editing, providing a unique model for studying gene function in a leukemic background.
CD1C encodes the CD1c glycoprotein, a member of the CD1 family that mediates lipid antigen presentation. CD1c heterodimerizes with ??2-microglobulin (B2M) and presents self and microbial lipid antigens to T cell receptors (TCR) on CD1c-restricted T cell subsets. TCR engagement activates the Src-family kinase LCK and the tyrosine kinase ZAP70, which phosphorylate the adaptor LAT, leading to PLC??1 activation and calcium flux. This cascade triggers the transcription factors NFAT and NF-??B, driving T cell proliferation and production of cytokines like IFN-?? and IL-4. CD1c expression is regulated by upstream signals including GM-CSF, IL-4, IFN-??, and Toll-like receptor (TLR) ligands, linking innate immune cues to adaptive T cell responses.
In the HAP1 cellular context, CD1C knockout eliminates CD1c-dependent lipid antigen presentation, providing a clean loss-of-function model for dissecting CD1c-mediated immune mechanisms. Because HAP1 cells are near-haploid, the CRISPR/Cas9-mediated disruption yields a uniform knockout population without allelic complexity. This model is particularly valuable for studying how lipid antigen presentation intersects with BCR-ABL1 signaling in CML, as HAP1 cells retain leukemic oncogenic pathways, enabling investigation of immune evasion strategies and nonclassical antigen presentation in hematological malignancies.
Researchers can employ these polyclonal knockout cells in various assays, including flow cytometry to confirm loss of CD1c surface expression, Western blotting and RT-qPCR for expression analysis, and co-culture experiments with CD1c-restricted T cells to measure T cell activation and cytokine release (IFN-??, IL-4) by ELISA. Lipid antigen presentation assays further assess pathway integrity. This product supports applications in immunology, antigen presentation studies, T cell biology, functional genomics, cancer immunotherapy, and drug target validation. For additional technical inquiries or experimental design support, please contact Ascent Research.
