The IL17RB Knockout A-549 Polyclonal Cells are a polyclonal population of A-549 human lung adenocarcinoma cells subjected to CRISPR/Cas9-mediated disruption of the IL17RB gene. This polyclonal knockout cell population provides a reliable loss-of-function model for dissecting IL17RB-dependent signaling pathways and cellular functions. By ablating expression of the IL-25/IL-17B receptor, this model allows precise interrogation of receptor-mediated responses in lung epithelial cells.
The A-549 cell line, derived from a human lung adenocarcinoma, exhibits epithelial morphology and serves as a model for alveolar basal epithelial cells and type II pneumocytes. It retains key features of lung adenocarcinoma, providing a relevant host for studying cancer biology and airway inflammatory responses. This genetic background offers a clinically meaningful context for evaluating IL17RB function in lung physiology and disease.
IL17RB encodes a single-pass transmembrane receptor that mediates signaling in response to the cytokines IL-17B and IL-25 (IL-17E). Ligand binding induces heterodimerization with the co-receptor IL17RA, leading to recruitment of the adaptor protein ACT1 (TRAF3IP2) and the E3 ubiquitin ligase TRAF6. Downstream signaling activates the IKK complex, triggering NF-??B nuclear translocation, and stimulates MAPK cascades including JNK, p38, and ERK. These pathways drive the transcriptional activation of pro-inflammatory genes, such as IL6, IL8, CXCL1, and CCL20, as well as Th2-type cytokines including IL4, IL5, and IL13. Upstream regulators such as TNF-?? and IL-1?? can also modulate IL17RB expression, providing additional layers of control. Through this signaling axis, IL17RB plays a critical role in Th2-type immunity, mucosal host defense, and chronic inflammatory responses.
In the A-549 lung epithelial context, IL17RB signaling is particularly relevant to inflammatory airway diseases. Activation of IL-25/IL-17RB has been implicated in asthma, allergic airway inflammation, and chronic rhinosinusitis, conditions in which airway epithelial cells are key effector sites. By using this knockout model, researchers can dissect the epithelial-intrinsic functions of IL17RB in driving cytokine and chemokine release, thereby clarifying its contribution to the recruitment and activation of immune cells such as eosinophils and Th2 cells. Moreover, given the role of IL17RB in lung adenocarcinoma microenvironments, this model facilitates studies of tumor-associated inflammation and potential therapeutic vulnerabilities.
This polyclonal knockout cell product is suited for a broad range of downstream applications. Western blotting and reporter assays can be used to assess NF-??B and MAPK pathway activation following stimulation with IL-25 or IL-17B. RT-qPCR and ELISA enable quantification of downstream cytokine expression, while flow cytometry and immunofluorescence confirm receptor surface loss and signaling complex dynamics. Co-immunoprecipitation experiments can probe IL17RB?CIL17RA interactions, and migration or invasion assays evaluate cell motility. The model supports drug screening efforts for asthma and allergic inflammation, validation of therapeutic targets in Th2-mediated diseases, and mechanistic studies of IL-25 signaling in lung cancer. For additional technical details, please contact Ascent Research.
