An autosomal recessive gene that delays expression of lupus in BXSB mice.
We report the generation and serologic, cellular, histologic, and genetic characteristics of a BXSB/MpJScr substrain, termed BXSB/MpJScr-ll/ll, that has lost early-life male lupus disease. Classic genetic analysis suggested that delayed disease expression results from the action of a single autosomal recessive gene. This putative gene, referred to as ll (long-lived), causes a significant delay in expression of autoimmune serology (total serum IgG and anti-nuclear antibodies levels), monocytosis, and of immune complex-mediated histopathologic changes such as glomerulonephritis, arteritis, and myocardial infarction. Presumably as a consequence of the delayed immunopathology male BXSB/MpJScr-ll/ll mice live three to four times longer than regular BXSB/MpJScr. This strain might be useful for analysis of single genes responsible for severe autoimmune disease expression.
Kofler
R
R
Department of Immunology, Scripps Clinic and Research Foundation, La Jolla, CA 92037.
McConahey
P J
PJ
Duchosal
M A
MA
Balderas
R S
RS
Theofilopoulos
A N
AN
Dixon
F J
FJ
D000818:Animals; D004279:DNA, Viral / Q000032:analysis; D004195:Disease Models, Animal; D005808:Genes, Recessive / Q000502:physiology; D020022:Genetic Predisposition to Disease; D008017:Life Expectancy; D008180:Lupus Erythematosus, Systemic / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D012190:Retroviridae / Q000235:genetics
D004279:DNA, Viral