Cd1d1/Cd1d2tm1Stst homozygous NOD congenic mice are viable, fertile, normal in size, and do not display any gross physical or behavioral abnormalities. The lack of CD1d expression on APC in homozygous mice was confirmed by FACS analysis. FACS analysis results also showed when compared to wildtype or heterozygous cohorts that CD1d deficient mice are characterized by a marked loss of NKT cells in spleen, pancreatic lymph nodes and pancreas; while there is an increase in the proportion of conventional T cells expressing CD25 and CD44 indicative of a memory phenotype. Conventional splenic T cells from wildtype or Cd1d deficient mice challenged with autoantigen GAD2 show no difference in proliferation or IL4, IFN-y and IL12 secretion. 50% of 15 week old Cd1d deficient mice are diabetic compared with 0% of wildtype controls and by 32 weeks of age 82% of the CD1d deficient mice are diabetic compared to 56% of the wildtype controls. This stock is useful in the study of Cd1d function in autoimmunity and peripheral tolerance.

These mice carry deletions of Cd1d1 and Cd1d2 and exhibit an accelerated onset and increased incidence of diabetes.

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

<a target="_blank" href="https://www.jax.org/jax-mice-and-services/customer-support" rel="noreferrer">Contact Customer Service</a> for more information.

NOD.129S6(B6)-Del(3Cd1d2-Cd1d1)1Sbp/SbwJ Frozen Embryos