The Importance of the Pathogenic 16/6 Idiotype in the Induction of SLE in Naive Mice

M. BLANK, M. KRUP, S. MENDLOVIC, H. FRICKE, E. MOZES, N. TALAL, A. R.M. COATES, Y. SHOENFELD

Research output: Contribution to journalArticlepeer-review

Abstract

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 an idiotype‐induced disease.

Original languageEnglish
Pages (from-to)45-52
Number of pages8
JournalScandinavian Journal of Immunology
Volume31
Issue number1
DOIs
StatePublished - Jan 1990

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