The CCL17 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 human near-haploid cell line, engineered to disrupt the CCL17 gene. This pooled model provides a robust loss-of-function system for studying CCL17 (TARC) chemokine biology without clonal isolation. The polyclonal format captures diverse editing events, avoiding clonal bias while maintaining target gene inactivation. Researchers can use these cells to examine how CCL17 secretion influences chemokine-mediated signaling and immune cell trafficking.
The HAP1 cell line is a near-haploid human line originating from the KBM-7 chronic myeloid leukemia line. Its adherent growth and predominantly haploid karyotype facilitate highly efficient CRISPR/Cas9 gene targeting, as single-allele modification suffices for functional knockout. Retaining fundamental signaling and secretion machineries, this hematopoietic progenitor-derived model is well-suited for biochemical and cell-based assays. The stable propagation of edited polyclonal pools ensures reproducible experimental setups without clonal isolation.
CCL17 is a chemoattractant that selectively binds the CCR4 receptor on Th2 lymphocytes and regulatory T cells, driving their directed migration. Its expression is upregulated by IL-4 and IL-13 via STAT6, as well as by NF-??B in response to TNF-alpha and IFN-gamma. Upon CCR4 binding, CCL17 initiates G-protein?Ccoupled signaling that engages PI3K/AKT and MAPK/ERK pathways, promoting chemotaxis. Interacting partners include G-protein subunits, beta-arrestins, and sulfated glycosaminoglycans, which fine-tune ligand presentation and receptor activity. In the knockout cells, abolished CCL17 production eliminates paracrine activation of CCR4 and downstream intracellular signals.
In the HAP1 background, the absence of CCL17 secretion establishes a clean baseline for dissecting the CCL17-CCR4 axis without interference from other chemokines. Unlike primary cells, HAP1 offers a consistent, scalable platform to study upstream regulators including IL-4/STAT6 and NF-??B. The knockout population can be used in conditioned media-based chemotaxis assays or co-cultures with CCR4-expressing reporter cells to measure migration deficits. This model is ideal for examining transcriptional control of CCL17 and for screening modulators that rescue or substitute its function, free from autocrine feedback.
Research applications include Th2 cell recruitment studies, modeling of allergic diseases (asthma, atopic dermatitis), and tumor microenvironment immunology. The cells enable chemotaxis assays, ELISA for CCL17 secretion, western blotting for phospho-ERK, RT-qPCR, flow cytometry for CCR4, and NF-??B reporter assays. These features support high-throughput screening for allergic inflammation and lymphoma therapies. For further information or to place an order, contact Ascent Research.
