Male mice on the BXSB recombinant inbred genetic background (see Stock No. 000740) develop spontaneous autoimmune disease closely resembling the human disease systemic lupus erythematosus (SLE), including moderate lymph node and spleen enlargement, hemolytic anemia, hypergammaglobulinemia, and immune complex glomerulonephritis. Homozygotes for the Tcratm1Mjo null allele lack alpha/beta T cells, which are essential for the development of the lupus-like autoimmune disease of Yaa-bearing males on the BXSB/MpJ background. Lacking alpha/beta T cells, these homozygotes do not develop anti-chromatin autoantibodies or hypergammaglobulinemia, do not develop glomerulonephritis, do not have the expanded Mac1+ MHC class II negative monocytosis, which is found in BXSB/MpJ males, but instead were found to survive 300 days essentially disease-free. Transfer of alpha/beta T cells from adult BXSB mice into these TCR alpha/beta null hosts conferred disease to the host even when the donor was female and therefore lacking the Yaa translocation (Lawson et al., 2001).
