Autoimmune abnormalities in a murine model of accelerated senescence.
Immunopathological abnormalities in senescence-accelerated mice (SAM) were studied by comparison of senescence-prone (SAM-P/1) and senescence-resistant (SAM-R/1) mice. Sera from SAM-P/1 mice contained a number of autoantibodies, including natural thymocytotoxic autoantibody (NTA), anti-nuclear antibodies (ANA) and IgG anti-single-stranded and anti-double-stranded (ss and ds) DNA antibodies. Furthermore, an earlier increase in serum IgG2 levels and an earlier appearance of IgG circulating immune-complexes (CIC) associated with low C3 levels, were observed in SAM-P/1 mice. These serological findings were distinctive features in SAM-P/1 mice, which could almost discriminate these mice from SAM-R/1 mice. In addition, age-associated glomerular mesangial and capillary lesions with granular IgG and C3 deposition were frequently observed in SAM-P/1 mice, whereas SAM-R/1 mice even at 10 months of age showed only mild mesangial lesions. These findings suggest that autoimmune abnormalities may contribute to the accelerated senescence in these mice.
Yoshioka
H
H
Department of Pathology, Faculty of Medicine, Kyoto University, Japan.
Yoshida
H
H
Doi
T
T
Muso
E
E
Ohshio
G
G
Higuchi
K
K
Inada
M
M
Miyake
T
T
Kita
T
T
Hamashima
Y
Y
D000375:Aging / Q000276:immunology* / Q000473:pathology; D000818:Animals; D000974:Antibodies, Antinuclear / Q000032:analysis; D000936:Antigen-Antibody Complex / Q000032:analysis; D000961:Antilymphocyte Serum / Q000032:analysis; D001323:Autoantibodies / Q000096:biosynthesis*; D003176:Complement C3 / Q000032:analysis; D004247:DNA / Q000276:immunology; D005260:Female; D005455:Fluorescent Antibody Technique; D007136:Immunoglobulins / Q000032:analysis; D007678:Kidney Glomerulus / Q000473:pathology; D051379:Mice; D008815:Mice, Inbred Strains; D011507:Proteinuria
D000974:Antibodies, Antinuclear; D000936:Antigen-Antibody Complex; D000961:Antilymphocyte Serum; D001323:Autoantibodies; D003176:Complement C3; D007136:Immunoglobulins; D004247:DNA