We have previously reported that CD4+ T cells recognizing a peptide comprising residues 234–252 of the heat shock protein (HSP) 70 of Mycobacterium tuberculosis (M. tb) in the context of RT1. B MHC class II molecule emerged in the peritoneal cavity during the course of Listeria monocytogenes infection in rats and suppressed the inflammatory responses against listerial infection via IL-10 production. We report in this work that pretreatment with peptide 234–252 of HSP70 derived from M. tb suppressed the development of adjuvant arthritis (AA) in Lewis rats induced using heat-killed M. tb. T cells from rats pretreated with peptide 234–252 produced a significant amount of IL-10 in response to the epitope. T cells from rats pretreated with the peptide and immunized with M. tb produced the larger amount of IL-10 in response to the peptide, but only a marginal level of IFN-γ in response to purified protein derivative of M. tb. Administration of anti-IL-10 Ab partly inhibited the suppressive effect of pretreatment with peptide 234–252 on the development of AA. Furthermore, transfer of a T cell line specific for the epitope at the time of AA induction markedly suppressed AA. These findings suggested that T cells recognizing peptide 234–252 may play a regulatory role in inflammation during AA via the production of suppressive cytokines including IL-10.