This double transgenic, targeted mutation strain carries a rearranged Tcr beta gene and a Tcr alpha gene from the pathogenic anti-insulin CD4+ T-cell clone BDC12-4.1 and NOD.Rag1tm1Mom targeted mutation (Stock No. <a href="https://www.jax.org/strain/003729">003729</a>). Triple mutant mice are viable and fertile. When the congenic NOD double transgenic is combined with a homozygous Rag1tm1Mom mutation, recombination of the endogenous TCR and immunoglobulin genes is prevented. As a result, mature T cells in these mice express only the BDC12-4.1 TCR. Further, approximately 50% of the TCR double transgenic, Rag1tm1Mom homozygote mice develop diabetes by 30 weeks of age. Histopathology indicates severe insulitis and/or destruction of all insulin-producing cells (Jasinski et al. 2006). This BDC12-4.1 TCR double transgenic, Rag1 deficient strain is useful for further studying the pathogenesis of insulin autoimmunity and diabetes. In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Mice of this BDC12-4.1 T-cell receptor (TCR) double transgenic, Rag1 deficient strain express only the BDC12-4.1 TCR, and are useful for studies regarding the pathogenesis of insulin autoimmunity and diabetes.

Typically mice are recovered in 12-16 weeks. Contact Customer Service to place an order or for more information.

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