In Nature this week, researchers from the University of Bonn and the University of California, Los Angeles, describe the use of a genetically engineered mouse to how melanomas become resistant to treatment. Adoptive cell therapies, which fight tumors with cytotoxic T cells, are often initially effective in treating melanoma, but patients frequently relapse. To find out why, the team established an effective adoptive cell therapy protocol in a mouse model of melanoma that that recapitulates tumor regression, remission, and relapse as seen in patients. They discovered that the cancer develops resistance through an inflammation-induced loss of melanocytic antigens, which the T cells use to identify tumors. They propose that future therapies should "simultaneously target melanocytic and non-melanocytic antigens to ensure broad recognition of both differentiated and de-differentiated melanoma cells."
Over in Nature Genetics, a multi-institutional team of researchers report on a genome-wide association study that has resulted in the discovery of new susceptibility loci for atopic dermatitis in the Japanese population. Looking at the more than 18,000 patient and controls, the researchers found eight new loci associated with the skin disorder at genome-wide significance, and replicated seven others previously reported. "Candidate genes at these loci suggest roles for epidermal barrier functions, adaptive immunity, IL-1 family signaling, negative regulation of apoptosis and the inflammatory response, regulatory T cells, and the vitamin D pathway in the pathogenesis of atopic dermatitis."