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Advances in understanding what stimulates autoantibodies to form and destroy tissues in lupus, rheumatoid arthritis and other systemic autoimmune diseases are announced in Nature (Vol. 416, No. 6881, dated 11 April 2002). The findings should open new avenues for treatment.
Ann Marshak Rothstein of Boston University School of Medicine, Massachusetts, and colleagues reveal an unexpected mechanism that explains how immune cells might perceive antibodies as pathogens, provoking the production of autoantibodies. They show that activation of autoreactive B cells involves the co-engagement of the B-cell receptor and a Toll-like receptor (TLR9) by antibody/autoantigen immune complexes. This establishes that endogenous TLR ligands have a critical role in the aberrant activation of the adaptive immune system.
"This raises the possibility that the drug chloroquine, which inhibits TLR9-mediated signalling, may be effective in some patients with systemic autoimmune diseases," explain Carola G. Vinuesa and Christopher C. Goodnow of the Australian National University, Canberra, in an accompanying News and Views article. "Drugs that specifically target Toll-like-receptor signalling pathways could be promising new treatments for antibody-mediated autoimmune diseases or their complications," they conclude.CONTACT:
Ann Marshak Rothstein
tel +1 617 638 4299
e-mail amrothst@bu.edu Christopher C. Goodnow
tel +61 2 6125 3621
e-mail chris.goodnow@anu.edu.au (C) Nature press release.
Message posted by: Trevor M. D'Souza
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