Antinuclear autoantibodies in flaky skin (fsn) mutant mice.
Mice homozygous.for the flaky skin (fsn) single gene mutation have a severe hyperproliferative disease resulting complex phenotype, which includes widespread inflammation and autoimmunity. Flaky skin mice have several serological and pathological features that share similarities with the human systemic autoimmune disease systemic lupus erythematosus (SLE). Analyses of the antinuclear and anti-dsDNA autoantibodies in fsn/fsn mice indicate that they are low titer IgG antibodies. These low titer anti-dsDNA autoantibodies can ultimately form immune complex deposition in the glomeruli associated kidney damage. IgE antibodies were identified in the immune complex deposition, however their role in the pathology is not determined. It is hypothesized that the mechanism of autoantibody production and autoimmune disease pathogenesis in mice homozygous for the fsn mutation is initiated by non-specific polyclonal activation of B-lymphocytes resulting in the synthesis of low affinity autoantibodies.
Withington
Susan
S
Department of Applied Medical Sciences, University of Southern Maine, Portland 04104-9300, USA.
Maltby-Askari
Ellen
E
Welner
Robert
R
Parker
Russ
R
Pelsue
Stephen C
SC
D000818:Animals; D000974:Antibodies, Antinuclear / Q000096:biosynthesis* / Q000097:blood; D004247:DNA / Q000276:immunology; D005455:Fluorescent Antibody Technique; D007073:Immunoglobulin E / Q000032:analysis; D015847:Interleukin-4 / Q000502:physiology; D051379:Mice; D008817:Mice, Mutant Strains; D011565:Psoriasis / Q000235:genetics / Q000276:immunology*
D000974:Antibodies, Antinuclear; D015847:Interleukin-4; D007073:Immunoglobulin E; D004247:DNA