The IL17RB Knockout HeLa Polyclonal Cells product comprises a population of HeLa cells subjected to CRISPR/Cas9-mediated gene disruption, providing a heterogeneous polyclonal knockout model for the human IL17RB gene. This polyclonal format is produced without single-cell cloning, yielding a cell pool that collectively exhibits targeted loss-of-function mutations. The edited population is designed for investigating IL17RB-dependent signaling events in a well-characterized epithelial cancer background, offering a versatile tool for high-throughput functional genomics, pathway dissection, and phenotypic screening applications in immunology and oncology research.
The host HeLa cell line is an immortalized, HPV18-positive cervical adenocarcinoma epithelial line that grows as an adherent monolayer. HeLa cells represent a classic in vitro model for studying epithelial cancer biology, signal transduction, and host-pathogen interactions. Their robust proliferation, ease of transfection, and extensive literature support make them a widely adopted substrate for gene-editing studies, facilitating the elucidation of oncogenic pathways and tumor microenvironment cross-talk. In the context of IL17RB knockout, HeLa cells provide a relevant backdrop to examine the receptor’s role in epithelial-derived pro-inflammatory responses and immune cell recruitment.
IL17RB encodes a receptor that specifically binds the cytokines IL-17B and IL-25 (also termed IL-17E), initiating intracellular signaling cascades that drive inflammation and immune activation. Ligand engagement promotes recruitment of the adaptor protein Act1 (TRAF3IP2) and the E3 ubiquitin ligase TRAF6, which together trigger downstream activation of the IKK complex and mitogen-activated protein kinases (MAPKs). These events culminate in the activation of transcription factors such as NF-??B and STAT3, which transcriptionally regulate an array of pro-inflammatory mediators including IL-6, IL-8, CXCL1, CCL20, and TNF-??. Additionally, JAK1 and JAK2 kinases have been shown to associate with IL17RB signaling, contributing to STAT3 phosphorylation and further amplifying the inflammatory gene expression program.
In the HeLa cell model, disruption of IL17RB abrogates the cellular response to IL-17B and IL-25, providing a clean loss-of-function system to dissect the receptor’s contribution to NF-??B and MAPK-driven transcription. Given that HeLa cells are derived from a cervical adenocarcinoma, this knockout model enables interrogation of IL17RB’s role in tumor-associated inflammation, a hallmark of cancer progression. It allows researchers to evaluate how the receptor modulates the secretion of cytokines and chemokines that shape the tumor microenvironment, such as IL-6 and CXCL1, and to assess crosstalk between epithelial cancer cells and immune components involved in chronic inflammatory conditions and cancer.
This IL17RB knockout polyclonal cell product is suitable for an array of experimental approaches, including western blotting for phospho-STAT3 and total STAT3, NF-??B luciferase reporter assays, real-time quantitative PCR measurement of IL-6 and IL-8 transcript levels, and ELISA-based quantification of secreted IL-6. Surface expression of IL17RB can be monitored by flow cytometry, and functional chemotaxis assays can be employed to study immune cell migration. Co-immunoprecipitation of Act1 further enables examination of signaling complex assembly. These tools support research into IL-17 family signaling, inflammation, cancer microenvironment studies, and drug target discovery. For additional product details and technical support, please contact Ascent Research.
