The possible roles of heat shock proteins in the pathogenesis of inflammatory arthritis have been discussed for a number of years, and investigated intensively in both animal models and human disease. This review surveys evidence which has pointed, on the one hand, to hsp as targets of a pathogenic immune response, and on the other, to an immunoregulatory role for T cell recognition of self hsp. The extent to which findings in experimental animals have led to further insights applicable to human disease is also emphasised.