Autoimmune arthritis is triggered by a systemic self-reactivity but why joints are the main targets for the specific inflammatory lesions remains unclear. Two papers in March 18 online Nature Immunology describe how antibodies to a ubiquitous cytoplasmic enzyme can provoke joint-specific autoimmune disease.

Isao Matsumoto and colleagues from Harvard Medical School examined the K/BxN mouse model, in which arthritis develops from pathogenic immunoglobulins (Igs) that recognize the ubiquitous cytoplasmic enzyme glucose-6-phosphate isomerase (GPI). They found an accumulation of extracellular GPI on the lining of the normal articular cavity, most visibly along the cartilage surface. In arthritic mice, these GPI deposits were amplified and localized with IgG and C3 complement. In addition, similar deposits were found in human arthritic joints (Nat Immunol 2002, DOI: 10.1038/ni772).

"As a result of these findings, we suggest a new model of arthritis pathogenesis, one that applies to disease in K/BxN mice but perhaps also...

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