The IL17RA Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from human Jurkat T lymphocytes. These cells contain a targeted disruption of the IL17RA gene, generating a loss-of-function model for interrogating interleukin-17 receptor A signaling.
Jurkat cells, an immortalized human T cell line from an acute lymphoblastic leukemia patient, serve as a widely used model for T cell activation and signaling. Their robust proliferative capacity and well-mapped signal transduction networks, particularly NF-??B and MAPK pathways, make them an ideal host for studying cytokine receptor functions.
IL17RA encodes a receptor subunit for the pro-inflammatory cytokines IL-17A, IL-17F, and the IL-17A/F heterodimer. Ligand engagement induces heterodimerization with IL-17RC, recruiting the adaptor ACT1 (TRAF3IP2) and the E3 ubiquitin ligase TRAF6, which in turn activate TAK1 and the IKK complex, leading to NF-??B nuclear translocation and activation of MAP kinases (ERK, JNK, p38). These pathways, together with C/EBP transcription factors, drive expression of pro-inflammatory mediators (IL-6, CXCL1, IL-8, CCL2, G-CSF, TNF) and antimicrobial peptides (beta-defensins). IL-17RA can also interact with IL-17RB and IL-17RE to mediate responses to other IL-17 cytokines. Disruption of IL17RA abolishes all IL-17-mediated signaling, impairing NF-??B, MAPK, and C/EBP pathway activation and consequently reducing the transcription of target genes, thereby dampening inflammatory responses.
In Jurkat T lymphocytes, IL-17RA is integral to mediating pro-inflammatory responses that are implicated in the pathogenesis of several autoimmune and chronic inflammatory conditions, including rheumatoid arthritis, psoriasis, multiple sclerosis, inflammatory bowel disease, and chronic mucocutaneous candidiasis. By knocking out IL17RA in this T cell model, researchers can specifically evaluate the contribution of T cell-intrinsic IL-17 receptor signaling to disease processes, isolating these effects from stromal or myeloid IL-17 responses. This focused system enables detailed analysis of how IL-17 cytokines directly influence T lymphocyte function and facilitates the development of targeted anti-inflammatory therapies.
This polyclonal knockout population is ideal for diverse functional studies, including dissection of IL-17 signaling networks in T cells, validation of drug targets, and screening for pathway modulators. Typical assays include western blotting and RT-qPCR for gene expression analysis, flow cytometry for phospho-NF-??B and phospho-MAPK, ELISA for secreted IL-6 and CXCL1, and NF-??B luciferase reporter assays to measure transcriptional activity. Co-immunoprecipitation can be used to assess disrupted interactions between IL-17RA and signaling partners such as ACT1 and TRAF6. Additionally, phospho-signaling arrays, migration studies, and drug sensitivity assays provide further functional readouts. For more details and ordering information, please contact Ascent Research.
