Extent of immune response associated with degree of inflammation and joint damage in rheumatoid arthritis
To diagnose rheumatoid arthritis, antibodies to the amino acid citrulline are commonly measured. A new study from Johan Rönnelidäs group at IGP shows that a broad mix of different antibodies in the joints is the dominant factor that can be associated with severe inflammation and joint damage. These findings, published in Annals of the Rheumatic Diseases, may eventually lead to improved diagnostics.
Rheumatoid arthritis (RA) is a chronic inflammatory disease that affects joints and other organs. To assist diagnosis of the disease, analysis of antibodies to the amino acid citrulline is performed. These ACPAs (anti-citrullinated protein antibodies), which form in response to inflammation. ACPAs can be demonstrated in roughly two-thirds of all patients with rheumatoid arthritis.
In the present study, Azita Sohrabian, PhD student in Johan Rönnelid’s group, has used a method of isolating immune complexes from various body fluids, and combined this with measurement of 19 ACPAs against various citrulline-containing protein fragments in serum and synovial fluid, and in immune complexes, from 77 RA patients.
The results confirmed that ACPAs can be pathogenic by forming immune complexes in the joints of RA patients, where these immune complexes can then cause joint inflammation. However, no single ACPA appears to be particularly important and instead a wide range of ACPAs in immune complexes from the joints seem to induce the local inflammation and drive the process of joint damage in RA. The findings correspond to what has previously been shown in antibody-induced joint inflammation in experimental animals, where various different antibodies to the same protein are required simultaneously to generate inflammation.