and DNA and the resultant inflammation can cause kidney damage, arthritis, and inflammation of the heart and blood vessels. Andrew Luster and colleagues from Harvard Medical School have shown that large aggregates of antibodyantigen complexes that contain DNA (known as DNA-containing immune complexes), isolated from the serum of lupus patients stimulate dendritic cells cells that identify foreign invaders and jumpstart the immune response. This series of events is dependent on the molecule known as Toll-like receptor 9 (TLR9). Interestingly, serum or immune complexes isolated from patients with other autoimmune rheumatic diseases did not have this effect. The authors found that this stimulation requires the presence of DNA as well as what is known as the Fc part of immunoglobulin G, and that stimulation of dendritic cells in this manner caused the production of many proinflammatory factors that likely contribute to the development of SLE.
The study will appear online on January 20 in advance of print publication in the February 1 edition of the Journal of Clinical Investigation.
TITLE: Human lupus autoantibodyDNA complexes activate DCs through cooperation of CD32 and TLR9.
Andrew D. Luster
Massachusetts General Hospital and Harvard University Medical School, Charlestown, Massachusetts USA.
Phone: 617-726-5710; Fax: 617-726-5651; E-mail: firstname.lastname@example.org.
View the PDF of this article at: https://www.the-jci.org/press/23025.pdf
From 5:00PM USA EST Thursday January 20, 2005 a PDF of this article will be available at: http://www.jci.org/papbyrecent.shtml
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Contact: Brooke Grindlinger
Journal of Clinical Investigation
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