The IL17RB Knockout TE1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from TE1, a human esophageal squamous cell carcinoma line. This product features disruption of the IL17RB gene, which encodes the receptor for IL-25 (IL-17E) and IL-17B. The polyclonal nature reflects a heterogeneous pool of edited cells, providing a physiologically relevant model without clonal selection artifacts. Designed for functional studies, these cells enable investigation of IL17RB-mediated signaling in an epithelial cancer background.
TE1 cells were established from a well-differentiated esophageal squamous cell carcinoma and are a standard in vitro model for esophageal cancer research. This adherent epithelial line retains properties of squamous cell carcinoma, including aberrant growth and invasive capacity. The esophageal cancer context is particularly pertinent because IL-25/IL17RB signaling contributes to inflammatory microenvironments and tumor progression. Knockout of IL17RB in this lineage allows dissection of receptor-specific effects on oncogenic and inflammatory pathways.
IL17RB functions as a receptor for IL-25 and IL-17B. Ligand engagement recruits the adaptor ACT1 (TRAF3IP2) and the ubiquitin ligase TRAF6, activating downstream kinases such as TAK1 and the IKK complex. This triggers NF-??B and MAPK pathways (ERK, JNK, p38), leading to transcriptional induction of pro-inflammatory mediators including IL-6, IL-8, and CXCL1. Thus, IL17RB is a critical node connecting IL-25 stimulation to inflammatory responses. Dysregulation of this axis is implicated in allergic inflammation, asthma, and cancer. The knockout model disrupts this signaling cascade, enabling precise dissection of IL17RB-dependent events.
In TE1 cells, IL17RB knockout attenuates IL-25-induced pro-inflammatory signaling, as the receptor is eliminated. This has direct relevance for esophageal squamous cell carcinoma and colorectal cancer, where IL-25/IL17RB interactions modulate immune cell infiltration and tumor cell behavior. The knockout cells allow assessment of NF-??B and MAPK activity, cytokine secretion, and cellular responses such as proliferation and migration in the absence of receptor function. This model helps clarify how IL17RB contributes to autocrine and paracrine loops within the tumor microenvironment, facilitating the identification of targetable vulnerabilities.
These polyclonal knockout cells support a variety of applications: Western blotting and RT-qPCR to verify knockout and downstream target expression; ELISA for cytokine profiling; and functional assays including proliferation, migration, and invasion. NF-??B reporter assays can monitor pathway activity. The model is suitable for target validation and mechanistic studies in inflammatory disease and cancer biology. For further inquiries, please contact Ascent Research.
