The interplay between genetic and environmental factors makes systemic lupus erythematosus (SLE) a complicated multifactorial autoimmune disease.
The hallmark of systemic lupus erythematosus (SLE) is the presence of high levels of anti-double-stranded DNA autoantibody (anti-dsDNA) in sera. In addition, greater infection rates are found in SLE patients and higher morbidity and mortality usually come from bacterial infections. Deciphering interactions between the susceptibility genes and the environmental factors for lupus complex traits is challenging and has resulted in only limited success.
In the June issue of Experimental Biology and Medicine Lee et al, from National Yang-Ming University in Taiwan, studied the role of anti-double stranded DNA (anti-dsDNA) and the Toll-like receptors (TLRs), TLR4 and TLR9, in the pathogenesis of lupus. They prepared transgenic mice carrying the anti-dsDNA transgene and challenged these mice with TLR4 and TLR9 agonists. They demonstrate that in the anti-dsDNA transgenic mice TLR4 and TLR9 are cooperatively linked to Lupus progression.
Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology and Medicine, said "These studies in transgenic mice offer new concepts for affecting immune tolerance and reducing SLE disease progression as future therapeutics are developed."