Mice homozygous for the severe combined immune deficiency spontaneous mutation (Prkdcscid, commonly referred to as scid) are characterized by an absence of functional T cells and B cells, lymphopenia, hypogammaglobulinemia, and a normal hematopoietic microenvironment. Normal antigen-presenting cell, myeloid, and NK cell functions are strain dependent. scid mice carry a DNA repair defect and a defect in the rearrangement of genes that code for antigen-specific receptors on lymphocytes. Most homozygotes have no detectable IgM, IgG1, IgG2a, IgG2b, IgG3, or IgA. Thymus, lymph nodes, and splenic follicles are virtually devoid of lymphocytes. scid mice accept allogeneic and xenogeneic grafts making them an ideal model for cell transfer experiments. Some scid mice will spontaneously develop partial immune reactivity. scid mice that have serum Ig levels greater than 1 ug/ml are considered "leaky." scid leakiness is highly strain dependent, increases with age, and is higher in mice housed under non-SPF conditions. In general, scid leakiness is high on the C57BL/6J and BALB/cBy genetic backgrounds, low on the C3H/HeJ background, and even lower on the NOD/ShiLtSz background. NOD/ShiLtSz-Prkdcscid mice are both insulitis- and diabetes-free throughout life and serve as a diabetes-free control for comparison to NOD/ShiLtJ mice (Stock No. 001976). Thymic lymphomas occur with high frequency, however, and life span typically is limited to only 8.5 months under specific pathogen-free conditions. In addition to being an excellent host for xenografts, NOD.CB17-Prkdcscid/J mice may be useful for delineation of the role of T cell subsets in autoimmune diabetes and also as a source for insulitis-free islets.
View Flow Cytometry Characterization Data for Immunodeficient JAX Strains
Body Weight Information - JAX® Mice Strain NOD.CB17-Prkdcscid/J (001303)
