Animal Models of Autoimmunity

Brown Norway Rat Model. Norway rats immunized with nontoxic concentrations of mercuric chloride (HgCl2) develop a disease characterized by Th2-cell-dependent B-cell stimulation. Stimulation culminates in the production of autoantibodies directed toward DNA, glomerular basement membrane, collagen IV, thyroglobulin, and myeloperoxidase.

The autoimmune disease is characterized by an autoimmune glomerulonephritis and immune complex vasculitis. Humans exposed to mercury develop the same kidney lesions. It is unclear whether this model can be used in the study of other chemicals.

Systemic Lupus Erythematosus. Three different models of spontaneous and two experimental SLE models have been described. The cross between New Zealand Black (NZB) and New Zealand White (NZW) yields hybrids that spontaneously develop a disease similar to human SLE. Hybrid BxSB mice also develop a lupuslike disease that occurs primarily in males. Mice carrying the Ipr gene on an MRL strain background also spontaneously develop SLE (Dixon, 1982).

SLE can also be experimentally induced in select mouse strains by the administration of anti-idiotypic antibodies or chronic GVH reactions (Gleichmann etal., 1984; Mendlovic etal., 1989).

Scleroderma. Two models, one spontaneous and one induced, of scleroderma have been reported in the literature. The spontaneous disease is found in inbred White Leghorn chickens (Gershwin etal., 1981). Scleroderma can also be induced in the rat following cyclosporin treatment or a GVH reaction (Bos et al., 1989; Furstetal., 1979).

Hemolytic Anemia. NZB mice spontaneously develop hemolytic anemia (Furst et al., 1979). Hemolytic anemia can also be induced in mice after treatment with levadopa (Sharon and Naor, 1989).

Thyroiditis. Spontaneous thyroiditis occurs in the OS chicken, Buffalo (BUFF) rat, and BB/W rat. Thyroiditis can be experimentally induced in mice, rats, guinea pigs, and rabbits (Kuppers etal., 1988).

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