The ERAP1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblastoid line, carrying a targeted disruption of the ERAP1 gene. This heterogeneous pool enables bulk functional assays without clonal selection bias.
Raji is an EBV-transformed human B lymphoblastoid line from Burkitt lymphoma, constitutively expressing MHC class I molecules. It serves as a well-characterized antigen-presenting cell model for adaptive immunity, widely used to study peptide loading, antigen processing, and T cell recognition.
ERAP1 is an IFN-??-inducible endoplasmic reticulum aminopeptidase that trims N-terminal residues of antigenic peptide precursors for optimal MHC class I binding. Its expression is upregulated by IFN-??, TNF-??, IL-1, and type I interferons. Within the peptide loading complex, ERAP1 interacts with ERAP2, MHC class I heavy chain, tapasin, calreticulin, ERp57, and ??2-microglobulin to shape the immunopeptidome and influence CD8+ T cell receptor and NK cell responses. In addition, ERAP1 processes angiotensin II and sheds cytokine receptors, releasing soluble TNF receptor 1 and soluble IL-6 receptor.
In Raji cells, ERAP1 knockout disrupts MHC class I antigen processing, altering peptide presentation and downstream T cell and NK cell activation. The polyclonal knockout format captures a range of editing efficiencies, reflecting biological heterogeneity and avoiding clonal selection artifacts. This model is especially relevant for studying B cell antigen presentation in autoimmune and cancer contexts.
Applications include immunopeptidomics (LC-MS/MS), flow cytometry for MHC class I surface expression, T cell activation assays (IFN-?? ELISpot), angiotensin II degradation measurements, and ELISA detection of soluble cytokine receptors. It is suited for mechanistic research on ankylosing spondylitis, psoriasis, Beh?et??s disease, type 1 diabetes, and for ERAP1 inhibitor screening in cancer immunotherapy. For further details, technical consultation, or a quotation, please contact Ascent Research.
