Antinuclear antibodies, drug-induced autoimmunity

The exact phenotype of the regulatory T cells in the case of low-dose D-penicillamine tolerance is not known, and non-lymphoid cells probably play a role as well. In another example of drug-induced autoimmune responses, the phenotype of regulatory T cells was identified as CD4+CD25+ (Layland et ah, 2004). In this study, CD4+CD25+ cells isolated from mice (A/J strain) exposed to procainamide, mercuiy(II) chloride, or gold salts were capable of preventing antinuclear antibody formation in similarly treated recipient mice, but also in mice subsequently treated with one of the other two chemicals. 

Dogs are a species frequently used in toxicity studies. However, there are only few reports in the open literature on dog studies with respect to chemical- or drug-induced hypersensitivity reactions or autoimmune effects, and studies are also often contradictory. For instance, procainamide has been shown to induce mainly an increase in antinuclear antibodies in one study (Balazs Robinson, 1983), but not in another study with younger dogs (Dubois Strain, 1972). Similar discrepancies were observed for hydralazine-induced effects in mice (Kammuller et al., 1989a). 

Autoimmune hepatitis (AIH). Chronic autoimmune-mediated hepatic inflammation characterized by antinuclear (ANA), smooth muscle (SMA)/anti-F-actin, liver-kidney microsomal (LKM), and soluble liver antigen (SLA) antibodies. Autoimmune hepatitis constitutes 10-20% of all cases of chronic hepatitis, ft may be idiopathic (Alff type 1, 2, and 3), part of autoimmune polyendocrine syndrome type 1 (APECED hepatitis), or drug-induced. See also -liver-kidney microsomal antibodies, liver-specific antigens. 

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