ANTI-DNA AUTOANTIBODIES STIMULATE THE RELEASE OF INTERLEUKIN-1 AND INTERLEUKIN-6 FROM ENDOTHELIAL CELLS

✍ Scribed by LAI, KAR NENG; LEUNG, JOSEPH C. K.; LAI, KA BIK; LI, PHILIP K. T.; LAI, CHRISTOPHER K. W.

• Publisher: John Wiley and Sons
• Year: 1996
• Tongue: English
• Weight: 649 KB
• Volume: 178
• Category: Article
• ISSN: 0022-3417
• DOI: 10.1002/(sici)1096-9896(199604)178:4<451::aid-path499>3.0.co;2-p

✦ Synopsis

The pathogenetic mechanism of vasculitis in systemic lupus erythematosus (SLE) remains a subject of debate. Evidence for a direct pathogenetic role of anti-double-stranded DNA antibodies (anti-dsDNA) is not strong. Supernatant concentrations of interleukin-1/3 and interleukin-6, and mRNAs encoding for interleukin-la and interleukin-1 receptor-1 were determined in cultured human umbilical vein endothelial cells (HUVEC), incubated with control IgG (n=18), anti-dsDNA (n=18), or IgG from the same lupus patient depleted of anti-dsDNA by affinity chromatography (anti-dsDNA-depIgG). Compared with control IgG, there was a significant increase of supernatant interleukin-1/? and interleukin-la mRNA in endothelial cells incubated with antidsDNA. The supernatant interleukin-la and interleukind, and mRNAs encoding for interleukin-la and interleukin-1 receptor-1, were significantly elevated in endothelial cells incubated with anti-dsDNA, compared with those incubated with anti-dsDNA-dep-IgG. Pretreating HUVEC with native DNA before incubating with antidsDNA did not result in an additive effect. These in vitvo studies suggest that anti-dsDNA plays an important pathogenetic role in inducing inflammatory injury of vascular endothelium in SLE.