We previously reported that transgenic mice carrying the human T cell leukemia virus type I (HTLV-I) env-pX region (pX-transgenic mice) develop rheumatoid-like inflammatory arthropathy, and suggested involvement of autoimmunity in the pathogenicity. In this report, to elucidate pathogenesis of the arthritis, we investigated arthritogenic antigens in the joints. The TCR beta-chain variable region (Vbeta) repertoires in the lymphatic organs were normal in transgenic mice, however, specific Vbeta-positive T cells were expanded oligoclonally in the affected joints, suggesting that specific antigens, but not superantigens, were involved in the expansion of these T cells. These expanded T cells had the same TCR as those of lymph node T cells reactive to type II collagen (IIC). Moreover, these mice were susceptible to IIC-induced arthritis and oligoclonal T cells of the same Vbeta specificity as that found in spontaneously developed arthritic joint accumulated in the arthritic joints after immunization with IIC. These observations show that endogenous IIC is one of the arthritogenic antigens in the joint, suggesting tolerance break to this antigen in pX-transgenic mice.