The IL17RA Knockout A-549 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population designed to eliminate functional interleukin-17 receptor A expression. Derived from the human A-549 lung adenocarcinoma epithelial cell line, this population has undergone CRISPR/Cas9-mediated disruption of the IL17RA gene, resulting in a loss-of-function model for IL-17 signaling. As a polyclonal population, the cells represent a heterogeneous pool of edited alleles, ensuring a robust ablation of the target protein without selection of a single clonal isolate. This product is ideal for researchers investigating the role of IL-17RA in epithelial inflammation, host defense, and downstream signaling pathways.
The A-549 cell line is a well-established model of type II pneumocyte-like alveolar epithelial biology, originally derived from a human lung carcinoma. These cells exhibit an epithelial morphology and are widely used to study lung adenocarcinoma biology, alveolar epithelial function, and inflammatory responses in a pulmonary context. Their endogenous expression of key signaling intermediates and responsiveness to exogenous cytokines make them a suitable platform for investigating IL-17RA-dependent pathways, particularly in the context of airway inflammation and respiratory infection.
IL17RA encodes the interleukin-17 receptor A subunit, which forms a heterodimeric complex with IL17RC to transduce signals from proinflammatory cytokines IL-17A and IL-17F. Ligand binding recruits the adaptor protein Act1 (TRAF3IP2), which in turn engages TRAF6 and activates downstream kinase cascades involving TAK1 and the IKK complex. This signaling leads to the activation of transcription factors NF-??B, AP-1, and C/EBP??, driving the expression of numerous proinflammatory mediators, including IL-6, IL-8 (CXCL8), CXCL1, CXCL2, TNF??, antimicrobial peptides such as ??-defensins, and the alarmins S100A8 and S100A9. Consequently, IL17RA knockout abrogates the cellular response to IL-17A/F, preventing Act1-mediated signal propagation and effectively silencing the NF-??B and MAPK pathways.
In A-549 cells, IL-17RA is functionally linked to the regulation of epithelial inflammatory responses and innate immunity. Disruption of this receptor in a lung epithelial context creates a powerful tool to dissect the contribution of IL-17 signaling to pulmonary inflammation and host defense against respiratory pathogens. Because A-549 cells retain key elements of the NF-??B and MAPK cascades, the knockout model allows unambiguous assessment of IL-17RA-dependent versus independent pathways. This is particularly relevant for diseases where aberrant IL-17 responses contribute to pathogenesis, such as asthma, chronic obstructive pulmonary disease, and acute respiratory distress syndrome, as well as for studying susceptibility to fungal and bacterial infections in the lung.
This polyclonal knockout cell population supports a broad range of experimental applications. It can be employed in cytokine stimulation assays followed by phospho-NF-??B analysis, RT-qPCR quantification of IL-6 and CXCL8 mRNA, ELISA-based measurement of secreted cytokines, and NF-??B reporter gene assays to directly monitor pathway activation. Further characterization may include western blotting for MAPK phosphorylation, immunofluorescence detection of p65 nuclear translocation, and flow cytometry for receptor expression. The cells are also valuable for functional studies such as cell migration and invasion assays, and for challenging with bacterial or fungal pathogens to examine IL-17RA-dependent host defense mechanisms. This product is thus ideal for studying IL-17-mediated lung inflammation, autoimmune disease research, and drug screening for novel IL-17 pathway inhibitors. For additional technical details, please contact Ascent Research.
