We have previously demonstrated the pathogenicity of the common anti‐DNA idiotype designated 16/6 Id. Immunization of naive mice with the 16/6 Id induced SLE‐like disease characterized by serological (e.g. anti‐dsDNA and anti‐Sm auto‐antibodies), clinical (increased ESR, leucopenia and proteinuria), and pathological (16/6 Id deposition in kidneys) parameters. To elucidate further the role of the 16/6 Id in SLE induction the following studies were carried out: BALB/c mice were immunized with SA‐1, a human anti‐DNA monoclonal antibody carrying the 16/6 Id; TB‐68, a mouse monoclonal anti‐tuberculosis (TB) glycolipid, which binds dsDNA and carries the 16/6 Id; TB‐72, a mouse monoclonal anti‐TB glycolipid that binds DNA and does not harbour the 16/6 Id; and 4B4, a human anti‐Sm antibody that carries the 16/6 Id. SLE was induced in BALB/c mice only when immunized with SA‐l, TB‐68, and 4B4, namely antibodies with diverse binding capacities albeit having the 16/6 Id. Our studies further support previous evidence on the pathogenic role attributed to the 16/6 Id in SLE, and suggest that SLE is most probably