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In rheumatoid arthritis (RA) the body’s immune system improperly identifies the synovial membrane in the joints as foreign and attacks it. Inflammation ensues, causing destruction of cartilage and tissues in and around the joints, and is associated with the influx of many types of immune cells such as CD4 T cells, B cells and macrophages. CD4 T cells have long been considered to play a central role in the origin and propagation of RA joint inflammation. However, recent research in mice suggests that although T cells initiate RA, it is antibodies that sustain the disease. These antibodies recognize a protein called GPI that is found throughout the body.
To date there has been no evidence that GPI is important in human rheumatoid arthritis. In the August issue of Nature Immunology (Vol. 2, No. 8, pp. 746-753), scientists from the Scripps Institute in California report that a high percentage of individuals with RA had increased concentrations of antibodies to GPI both in the sera and the synovial fluid in the joints. In addition, high concentrations of the protein itself were found on the surface lining the joints. These results suggest that the immunological events that lead to the development of autoimmune diseases in the mouse model may also take place in humans. This could help the development of new strategies for therapeutic intervention. Henrik Ditzel
Scripps Research Institute
10550 North Torrey Pines Road
La Jolla, CA 92037
UNITED STATES
Tel: (+1) 858-784-8157
Fax: (+1) 858-784-8360
hditzel@scripps.edu (C) Nature Immunology press release.
Message posted by: Trevor M. D'Souza
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