The study investigates the cloning and characterization of a mycobacterial epitope recognized by T lymphocytes in adjuvant arthritis (AA). AA is a chronic disease in rats induced by immunization with *Mycobacterium tuberculosis* (Mt) antigens. The researchers isolated arthrogenic T-cell lines and clones, which demonstrated cross-reactivity between the critical *M. tuberculosis* antigen and a self-antigen in joint cartilage. Patients with rheumatoid arthritis also showed specific T-lymphocyte reactivity to the *M. tuberculosis* fraction containing this cross-reactive epitope. To identify the critical epitope, the researchers used AA T-cell clones to screen mycobacterial antigens expressed in *Escherichia coli* and genetically engineered truncated proteins and synthetic peptides. The clones recognized an epitope formed by amino acids at positions 180–188 in the sequence of a *Mycobacterium bovis* BCG antigen. Administration of this antigen to rats induced resistance to subsequent attempts to produce AA. The study also explored the role of the 65K protein, a heat-shock protein, in AA. The 65K antigen, when administered to rats, did not induce AA but provided resistance to subsequent attempts to induce AA by immunization with whole Mt. This suggests that the 65K antigen may activate suppressor-inducer T cells, leading to resistance to AA. Additionally, the researchers found that the 65K antigen could be a specific target for T-lymphocyte recognition in patients with rheumatoid arthritis. The 65K antigen is related to other shared antigens in various mycobacteria and may play a role in the pathogenesis of AA.The study investigates the cloning and characterization of a mycobacterial epitope recognized by T lymphocytes in adjuvant arthritis (AA). AA is a chronic disease in rats induced by immunization with *Mycobacterium tuberculosis* (Mt) antigens. The researchers isolated arthrogenic T-cell lines and clones, which demonstrated cross-reactivity between the critical *M. tuberculosis* antigen and a self-antigen in joint cartilage. Patients with rheumatoid arthritis also showed specific T-lymphocyte reactivity to the *M. tuberculosis* fraction containing this cross-reactive epitope. To identify the critical epitope, the researchers used AA T-cell clones to screen mycobacterial antigens expressed in *Escherichia coli* and genetically engineered truncated proteins and synthetic peptides. The clones recognized an epitope formed by amino acids at positions 180–188 in the sequence of a *Mycobacterium bovis* BCG antigen. Administration of this antigen to rats induced resistance to subsequent attempts to produce AA. The study also explored the role of the 65K protein, a heat-shock protein, in AA. The 65K antigen, when administered to rats, did not induce AA but provided resistance to subsequent attempts to induce AA by immunization with whole Mt. This suggests that the 65K antigen may activate suppressor-inducer T cells, leading to resistance to AA. Additionally, the researchers found that the 65K antigen could be a specific target for T-lymphocyte recognition in patients with rheumatoid arthritis. The 65K antigen is related to other shared antigens in various mycobacteria and may play a role in the pathogenesis of AA.