Knocking The SOCS Off Rheumatoid Arthritis

Main Category: Arthritis / Rheumatology
Article Date: 20 May 2006 - 9:00 PDT

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Rheumatoid arthritis is an autoimmune disease that causes chronic inflammation of the joints and occurs when the body's tissues are mistakenly attacked by its own immune system. A study by Ian Wicks and colleagues from the Walter and Eliza Hall Research Institute, Australia, appearing online on May 18 in advance of print publication in the June issue of the Journal of Clinical Investigation, is the first analysis of the function of the SOCS-3 molecule in a mouse model of inflammatory arthritis.

The authors used a conditional gene deletion strategy to delete SOCS-3 only in hematopoietic and endothelial cells of mice. Joint inflammation in these mice was particularly severe and characterized by increased numbers of neutrophils in the inflamed joints, bone marrow, blood, and spleen. Local bone breakdown and T cell production were also dramatically increased in the absence of SOCS-3. SOCS-3 appeared to be directly induced by IL-1 in macrophages. These results led to the conclusion that SOCS-3 is an important molecule implicated in arthritis and that pharmacological manipulation of SOCS-3 might be a novel therapeutic strategy to block multiple inflammatory pathways during autoimmune-mediated, inflammatory diseases.

TITLE: SOCS-3 negatively regulates innate and adaptive immune mechanisms in acute IL-1-dependent inflammatory arthritis.

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the-jci.org/article.php?id=25660

Brooke Grindlinger
press_releases@the-jci.org
Journal of Clinical Investigation
http://www.jci.org

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