Dermatomyositis is a connective-tissue disease that is characterized by inflammation of the skin and the muscles. Exposure to sunlight, either occupationally or recreationally, is anecdotally associated with flare-ups and even with onset of the condition in some cases. Inspired by those stories, Frederick Miller, chief of the environmental autoimmunity group at the National Institutes of Health, and his colleagues performed the first worldwide evaluation of dermatomyositis to determine whether ultraviolet radiation could explain variations in the frequency of disease.

"We did an evaluation of many centers around the world and found that the proportion of patients who have dermatomyositis or the anti-Mi-2 autoantibody strongly correlated with the amount of UV light measured at that location," says Miller. In contrast, the frequency of a closely related autoimmune muscle disease, polymyositis, was inversely correlated with ultraviolet radiation, says Miller.

HLA-DRB1 gene variants are common in autoimmune disorders, but their precise roles are not always known. The Mi-2 autoantibody is associated with the HLA-DRB1*0701 gene in European Americans and with HLA-DRB1*0302 in African Americans, according to Miller (T.P. O'Hanlon et al., "HLA polymorphisms in African Americans with idiopathic inflammatory myopathy: Allelic profiles distinguish patients with different clinical phenotypes and myositis autoantibodies," Arthritis Rheum, 54:3670-81, 2006.) The proteins encoded by these two genes share a sequence motif, which is predicted by computer modeling to have identical 3-dimensional orientations with the critical peptide-binding groove. Nonetheless, the mechanisms that might trigger expression of dermatomyositis or anti-Mi-2 autoantibodies in carriers of the risk factor genes are still not clear.