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Tolerization of B10.RIII mice (H-2r) with intravenously injected type II collagen (CII) renders the animals resistant to induction of collagen-induced arthritis (CIA). In order to clarify 11-2r- restricted T-cell responses that modulate CIA, we have analysed the T-cell proliferative response of B10.RIII mice against cyanogen bromide (CB) peptides of CII, and detected the strongest response to α(II)-CB10 (CII 552–897). A panel of chemically synthesized overlapping peptide homologues was used to deduce the minimum structure of this determinant which was found to be CII 610–618. A 15-residue synthetic peptide flanking this region. CII 607–621, was found to effectively suppress arthritis when administered as a tolerogen. Collectively, these data identify the structural component within α1(II)-CB10 which is capable of inducing tolerance in BIO.RIII mice. A similar approach to the treatment of autoimmune arthritis, involving the institution of self-tolerance, has potential applicability to human rheumatoid arthritis. [ABSTRACT FROM AUTHOR]