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The Brown-Norway rat is prone to atopy; after intraperitoneal challenge with allergen it produces lots if IgE, develops eosinophilia, and shows early and late bronchospasm. Research workers in Taiwan (Ching-Hsiang Hsu and colleagues, Nature Medicine 1996;2:540-4) injected a plasmid DNA encoding a house dust mite allergen into the muscles of such mice. They showed that the muscle cells then produced the allergen for at least six months and that the rats produced IgG but not IgE specific antibodies. When later challenged with the allergen they produced only 20% of the allergen specific IgE produced by control rats similarly challenged and, unlike control rats, they did not develop bronchospasm or release large amounts of histamine into their lungs. This inhibition of response was specific to the house dust mite allergen, the rats responding as usual to a different allergen. Furthermore the response inhibition was transferred to immunologically naive rats by injecting them with CD8+T cells from the experimental rats. Intracellular and extracellular antigens are dealt with differently. Peptides from intracellular antigens are presented to CD8+T cells by major histocompatibility complex class I molecules present on all cells whereas those from extracellular antigens are presented to CD4+T cells by MHC class II molecules on specialised cells. This may explain why persuading somatic cells to produce an allergen might alter the immune response to that allergen. There is much to be learned before this work can be translated to therapeutic use. There are fears of potential carcinogenesis because of interference with normal genes and it is not known how animals (or people) already sensitised to allergen would respond. It’s fascinating, though, isn’t it?