CBA/N X-linked defect delays expression of the Y-linked accelerated autoimmune disease in BXSB mice.
BXSB male mice spontaneously develop progressive autoimmune disease characterized by high serum immunoglobulins, including anti-nuclear antibodies (ANA), enlarged spleen and lymph nodes, and diffuse proliferative glomerulonephritis. Females develop symptoms at a much slower rate. The mechanisms underlying the autoimmune disease and the nature of the Y-linked accelerating factor have not yet been elucidated. We found that the male progeny of the cross between the non-autoimmune strain CBA/Ca and BXSB (CBA/Ca X BXSB)F1 showed progressing signs of autoimmunity starting at 6 to 7 mo. In contrast, the male progeny that resulted from BXSB males crossed with immune-defective CBA/N females (Xid) were devoid of splenic B colonies, were nonresponsive to TNP-Ficoll, and were free of autoimmune disease for at least 10 mo. At 18 mo, some of the (CBA/N X BXSB)F1 mice developed weak antinuclear antibodies, but no spleen or lymph node enlargement was seen. The same mice had low anti-TNP Ficoll responses but did not produce B colonies in vitro. The role of the X chromosome in regulating expression of autoimmunity in young and old BXSB mice is discussed.
D000375:Aging; D000818:Animals; D001327:Autoimmune Diseases / Q000235:genetics* / Q000276:immunology / Q000503:physiopathology; D001402:B-Lymphocytes / Q000166:cytology; D002454:Cell Differentiation; D003433:Crosses, Genetic; D005260:Female; D008198:Lymph Nodes / Q000033:anatomy & histology; D008297:Male; D051379:Mice; D008808:Mice, Inbred CBA / Q000235:genetics*; D008817:Mice, Mutant Strains / Q000235:genetics*; D009929:Organ Size; D012730:Sex Chromosomes; D013154:Spleen / Q000033:anatomy & histology; D014960:X Chromosome; D014998:Y Chromosome