Orders by weight:
- The B2m-NOG is an immunodeficient CIEA NOG mouse® with an additional knockout of the B2m gene which disrupts MHC class I antigen presentation.
- B2m-NOG mice can successfully engraft human PBMCs and tumors.
- Compared to NOG, B2m-NOG mice have markedly delayed GvHD onset after human PBMC engraftment, providing an expanded study window (8+ weeks). This vastly increases the utility of the model in immuno-oncology experiments.
- B2m-NOG has reduced efficiency of human PBMC engraftment relative to NOG as well as a CD4+ bias that increases over time in engrafted peripheral blood T cells (see data section).
- Available engrafted with human PBMCs as huPBMC-B2m-NOG.
Taconic cannot accept orders by weight for this model. Please note that shipments may contain animals with a larger weight variation.
Origin: The CIEA NOG mouse® was developed by Mamoru Ito of the Central Institute for Experimental Animals (CIEA) in Japan. The Prkdcscid mutation was identified by Mel Bosma of the Fox Chase Cancer Center in a C.B-17 congenic mouse population. This mutation was backcrossed onto the NOD/ShiJic strain at CIEA for at least eight generations. The Il2rg targeted mutation was developed by Dr. Kazuo Sugamura of Tohoku University by targeting the gene in ES cells derived from a 129 strain. Targeted ES cells were injected into C57BL/6 blastocysts. Resultant chimeras were backcrossed onto the C57BL/6JJic background for at least eight generations. The CIEA NOG mouse® was developed by backcrossing the C57BL/6JJic-Il2rg line to the NOD/ShiJic-Prkdcscid line for a total of eight generations. The B2m gene was knocked out via CRISPR-mediated knock-in of a nonsense mutation into exon 1. This mutation was made directly in the NOG strain.
Availability: Available now in typical study quantities.