The genetic regulation of the induction of experimental SLE

• Published in: Immunology 1990-02, Vol.69 (2), p.228-236
• Main Authors: MENDLOVIC, S, BROCKE, S, FRICKE, H, SHOENFELD, Y, BAKIMER, R, MOZES, E
• Format: Article
• Language: English
• Subjects: Animals; Antibodies, Anti-Idiotypic - biosynthesis; Antibodies, Antinuclear - immunology; Antibodies, Monoclonal - immunology; Biological and medical sciences; Experimental and animal immunopathology. Animal models; Genetic Predisposition to Disease; Immunization; Immunoglobulin Idiotypes - immunology; Immunopathology; Lupus Erythematosus, Systemic - genetics; Lupus Erythematosus, Systemic - immunology; Medical sciences; Mice; Mice, Inbred Strains
• ISSN: 0019-2805; 1365-2567

We have recently reported the induction of systemic lupus erythematosus (SLE) in C3H.SW female mice by their immunization with a human monoclonal anti-DNA antibody that bears a common idiotype termed 16/6 Id. In the present study, the ability to induce experimental SLE in seven inbred mouse strains by immunization with the 16/6 Id was examined. Two out of the seven strains failed to develop the disease. These two strains did not produce antibodies specific to the 16/6 Id, while the other five strains produced high titres of anti-16/6 Id antibodies. The anti-16/6 Id antibody response, followed by the induction of the disease, was not found to be MHC or Ig heavy chain allotype linked. F1 hybrids between a resistant strain and two of the susceptible strains were found to be resistant to the induction of the disease, indicating that susceptibility is inherited as a recessive trait. In the autoimmune NZB/W F1 female mice, immunization with the 16/6 Id resulted in an early onset of the SLE-like disease. The results of the present study indicate the role of the anti-16/6 Id antibodies in the induction of experimental SLE, and provide direct evidence for the importance of the genetic background in determining susceptibility to SLE.