The CD1B Knockout HAP1 Polyclonal Cells product provides a heterogeneous pool of CRISPR/Cas9-edited HAP1 cells harboring targeted disruption of the CD1B gene. This polyclonal knockout cell population serves as a ready-to-use loss-of-function model for studying CD1-mediated lipid antigen presentation and its role in innate and adaptive immunity. The polyclonal format ensures a broad representation of knockout alleles, enabling robust functional studies without clonal bias.
HAP1 is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia cell line, originally isolated from a male patient. Its near-haploid karyotype simplifies genetic analysis and facilitates high-efficiency gene editing, making it a preferred model for knockout studies. HAP1 cells retain key cellular machineries, including endosomal trafficking pathways, relevant for CD1B biology.
CD1B is a non-classical MHC class I-like glycoprotein that mediates presentation of lipid and glycolipid antigens, including mycolic acids from Mycobacterium tuberculosis, to CD1-restricted T cells. It is regulated upstream by GM-CSF, IL-4, PPAR??, and TLR agonists. Upon lipid loading in endosomal compartments, facilitated by the AP-3 complex and Saposin C, CD1B forms a complex with ??2-microglobulin and traffics to the cell surface. Engagement with the T cell receptor (TCR) on specific T cells triggers downstream signaling, leading to IFN-?? secretion, IL-4 secretion, and T cell proliferation. This axis bridges innate recognition of microbial lipids with adaptive cytokine responses, critical in host defense against mycobacteria.
In HAP1 cells, CD1B knockout disrupts the presentation of lipid antigens, enabling precise dissection of CD1B-dependent immune activation pathways. This model is particularly valuable for investigating mycobacterial antigen processing, as HAP1 cells express the necessary endosomal machinery for lipid loading. By comparing wild-type and CD1B-knockout populations, researchers can assess the contribution of CD1B to T cell activation and cytokine production in response to lipid antigens. The near-haploid background reduces genetic redundancy, sharpening the resolution of phenotypic analyses.
This knockout cell pool is suited for a range of experimental applications, including lipid antigen presentation assays using IFN-?? ELISpot readouts, flow cytometric analysis of CD1B surface expression, co-immunoprecipitation studies with ??2-microglobulin, and confocal imaging of endosomal trafficking. It supports drug screening for tuberculosis and host?Cpathogen interaction studies. Researchers investigating psoriasis or autoimmune diseases may also utilize this model to explore aberrant lipid antigen presentation. For custom experimental protocols or further product information, please contact Ascent Research.
