One of the best examples of a gene-environment interaction in autoimmunity involves instances in which certain drugs produce a lupus-like syndrome in genetically susceptible individuals. It turns out that people who carry a variant of the N-acetyltransferase-2 gene, so-called slow acetylators, do not metabolize the drugs procainamide and hydralazine very well. Thus, they are predisposed to lupus induced by these drugs because these substances remain active for extended periods in the body. Removing the drugs, however, eliminates the autoimmunity.

Although the mechanisms that cause drug-induced lupus are believed to be somewhat different from those of systemic lupus erythematosus (SLE), the similarities encouraged some investigators to look for a connection. According to Bruce Richardson, a professor of medicine at the University of Michigan Medical...

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