The HLA-DRA Knockout 143B Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the 143B human osteosarcoma line, established through targeted disruption of the HLA-DRA gene. This heterogeneous knockout pool provides a loss-of-function model for the alpha chain of the MHC class II molecule HLA-DR, avoiding clonal selection artifacts.
The 143B cell line is a highly tumorigenic and metastatic human osteosarcoma model, originating from a primary bone tumor. These transformed osteoblast-like cells exhibit rapid proliferation, invasiveness, and robust tumor formation in vivo, making them a standard platform for bone cancer biology and immuno-oncology investigations.
HLA-DRA encodes the invariant ?? subunit of the HLA-DR heterodimer, which pairs with HLA-DRB chains and the invariant chain CD74 to load antigenic peptides for CD4+ T cell presentation. Transcription is controlled by CIITA and the RFX complex downstream of IFN-??/JAK-STAT signaling. Surface HLA-DR engagement with TCR/CD4 on T cells triggers activation and differentiation into Th1, Th2, or Th17 helper subsets, while HLA-DM and HLA-DO catalyze peptide exchange in endosomes. Through these interactions, HLA-DRA is central to initiating adaptive immunity.
In the 143B osteosarcoma context, HLA-DRA knockout eliminates MHC II surface expression, preventing exogenous antigen presentation and recapitulating immune evasion strategies used by tumors. Given that osteosarcomas frequently downregulate MHC II to escape CD4+ T cell surveillance, this model is valuable for dissecting how such loss impacts tumor immunogenicity, metastatic behavior, and response to immunotherapies.
This polyclonal knockout cell pool is ideal for studying tumor immune escape, MHC class II deficiency, autoimmunity, and transplant rejection mechanisms. Representative applications include flow cytometry to confirm MHC II loss, western blotting of HLA-DR subunits, antigen presentation assays with peptide-pulsed cells, and T cell activation or cytokine release co-culture experiments. It also supports screening of agents that reinstate MHC II expression. For additional information, please contact Ascent Research.
