Experimental
systemic lupus erythematosus (SLE) can be induced in mice by immunization with a human monoclonal anti-
DNA Ab, bearing a major Id 16/6Id. Immunized mice initially produce Abs to 16/6Id,
DNA and nuclear Ags, and subsequently develop various clinical manifestations including
leukopenia and renal
immune complex disease. MHC class I Ags play a critical role in the induction and progression of experimental SLE. The present study reports that ocular changes also occur in mice with experimental SLE. The ocular disease is characterized by bilateral subacute and chronic
inflammation of the eyelids (
blepharitis) with
immune complex IgG deposition and hypertrophic meibomian glands. The severity of ocular changes was strain dependent: most severe in 129 mice, less intense in BALB/c animals and only minimal in C3H.SW mice. No
blepharitis developed in mice deficient in MHC class I expression. Further, the disease was strongly inhibited in BALB/c mice treated with
methimazole, an agent that has been shown to repress transcription of MHC class I. In these cases, there was no
IgG deposition and a decreased infiltration of inflammatory cells in the eyelids. These observations thus suggest that, similar to the observation with experimental SLE, MHC class I is critical in the onset of this experimental autoimmune
blepharitis. The new experimental
eye disease described here provides an animal model for chronic
blepharitis in humans, a common condition for which such a model has been sought.