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- Title
Spontaneous Autoimmune Skin Lesions of MRL/n Mice: Autoimmune Disease-Prone Genetic Background in Relation to Fas-Defect MRL/1pr Mice.
- Authors
Furukawa, Fukumi; Kanauchi, Hideo; Wakita, Hisashi; Tokura, Yoshiki; Tachibana, Takao; Horiguchi, Yuji; Imamura, Sadao; Ozaki, Shouichi; Takigawa, Masahiro
- Abstract
The autoimmune-prone MRL/Mp-<em>lpr/lpr</em> (MRL/lpr) mouse is characterized by the <em>lpr</em> mutation, which is a defect in the Fas antigen. Since Fas mediates apoptosis, this defect results in CD4-CD8- double negative T-cell proliferation, lupus nephritis, and macroscopic lupus erythematosus-like skin lesions. The control counterpart of MRL/lpr mouse is the MRL/Mp-+/+ (MRL/n) mouse, which lacks the <em>lpr</em> mutation and is almost normal during the first 6 mo of life. The lpr mutation, however, accelerates autoimmune phenomena in MRL/lpr mice. Thus, it is important to investigate autoimmune diseases like systemic lupus erythematosis in relation to the autoimmune disease-prone genetic background of MRL/n mice. We found that skin lesions in aged MRL/n mice had unique characteristics. The first characteristic is spontaneous occurrence, and the second is epidermal cell nuclear immunostaining with IgGs by direct immunofluorescence. The skin lesions in aged MRL/n mice showed milder inflammation than in MRL/lpr mice. A homogeneous pattern of epidermal cell nuclear staining was always associated with nuclear staining in kidney cells and also correlated with the <em>in vitro</em> binding of sera to keratinocytes cultured from newborn MRL/n mice. These results suggest that the skin lesions of aged MRL/n mice are a good model for certain types of cutaneous lupus erythematosus and also can provide new insights into the long-standing controversy whether epidermal cell nuclear staining occurs <em>in vivo</em>.
- Subjects
LUPUS erythematosus; SKIN diseases; AUTOIMMUNE diseases; CONNECTIVE tissue diseases; APOPTOSIS; CELL death
- Publication
Journal of Investigative Dermatology, 1996, Vol 107, Issue 1, p95
- ISSN
0022-202X
- Publication type
Article
- DOI
10.1111/1523-1747.ep12298305