The past year has seen advances in our understanding of the mechanisms that control the expression of organ-specific autoimmunity. Attempts to develop therapeutic strategies for the prevention of autoimmune disease have largely been based on deviation of the T-cell response away from an autoaggressive, pro-inflammatory Th1 response. Manipulation of the cytokine environment at the site of antigen uptake or presentation, the source of endogenous antigen, costimulatory molecules or peptides processed and presented has yielded interesting results.