Organ-specific autoimmune diseases are mediated by interferon gamma (IFN-gamma)-producing T helper 1 (Th1) cells. Here, Martin Röcken and colleagues review the experimental basis for an antigen-specific therapeutic approach to inflammatory autoimmune diseases. This strategy involves selective deviation of harmful Th1 responses towards an anti-inflammatory, interleukin 4 (IL-4)-producing Th2 phenotype.