Abstract
Autoimmune inflammatory diseases occur commonly in Western populations and include conditions such as juvenile-onset diabetes mellitus, rheumatoid arthritis, inflammatory bowel disease and systemic lupus erythematosus. The precise cause of these diseases remains enigmatic. However, current notions of pathogenesis support an important interplay between host genetics and acquired, or environmental, factors. From an immunologic perspective, autoimmune inflammatory diseases develop as a result of a loss of immune tolerance and the initiation of immune-mediated tissue injury. In the following review, we discuss recent studies pointing to an important role for the upstream mediator macrophage migration inhibitory factor in the effector responses producing autoimmune tissue damage.