The CD58 Knockout 22Rv1 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human 22Rv1 prostate carcinoma epithelial cell line, in which the CD58 gene has been disrupted through CRISPR/Cas9-mediated gene editing. This heterogeneous pool provides a loss-of-function model for investigating CD58-dependent processes in an androgen-responsive prostate cancer background, without clonal isolation.
The 22Rv1 cell line is a well-characterized model of prostate adenocarcinoma, originally established from a CWR22 xenograft. It retains wild-type androgen receptor expression and responsiveness, making it a standard tool for studying androgen signaling and the progression to castration-resistant prostate cancer. These adherent epithelial cells maintain key features of tumor biology, including androgen-driven transcriptional programs, enabling physiologically relevant immune interaction studies.
CD58 (lymphocyte function-associated antigen 3) is a GPI-anchored adhesion molecule that serves as the primary ligand for CD2, providing co-stimulatory signals essential for T cell activation. CD2 engagement triggers phosphorylation of PLCgamma1 and activates MAPK cascades, leading to IL-2 production and proliferation. This signaling is mediated by early kinases Lck and ZAP70 and the adaptor protein LAT. CD58 expression is induced by TNF-alpha and IFN-gamma through NF-kB, placing it under inflammatory control and highlighting its role in fine-tuning immune responses.
In 22Rv1 prostate cancer cells, CD58 disruption provides a model to study how tumor cells influence T cell activity. Loss of CD58 may impair immunological synapse formation and T cell activation, potentially contributing to immune evasion in the tumor microenvironment. This model supports investigations into CD58-dependent immune modulation under both androgen-responsive and castration-resistant conditions, aiding the identification of strategies to restore anti-tumor immunity.
Key applications include co-culture with T lymphocytes to assess adhesion, synapse assembly, and cytokine secretion by ELISA. Surface CD58 loss can be confirmed by flow cytometry, while western blotting and RT-qPCR monitor downstream signaling changes. T cell proliferation assays measure functional co-stimulatory capacity. These assays enable interrogation of immune escape mechanisms in prostate cancer and evaluation of CD58 as an immunotherapeutic target. For further information, contact Ascent Research.
