Synovial fibroblasts spread rheumatoid arthritis to unaffected joints
By S. Lefèvre, A. Knedla, Christoph Tennie, A. Kampmann, C. Wunrau, R. Dinser, A. Korb, Eva-Maria Schnäker, I. Tarner, P. Robbins and 8 more. Nature Medicine, 2009
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Active rheumatoid arthritis originates from few joints but subsequently affects the majority of joints. Thus far, the pathways of the progression of the disease are largely unknown. As rheumatoid arthritis synovial fibroblasts (RASFs) which can be found in RA synovium are key players in joint destruction and are able to migrate in vitro, we evaluated the potential of RASFs to spread the disease in vivo. To simulate the primary joint of origin, we implanted healthy human cartilage together with RASFs subcutaneously into severe combined immunodeficient (SCID) mice. At the contralateral flank, we implanted healthy cartilage without cells. RASFs showed an active movement to the naive cartilage via the vasculature independent of the site of application of RASFs into the SCID mouse, leading to a marked destruction of the target cartilage. These findings support the hypothesis that the characteristic clinical phenomenon of destructive arthritis spreading between joints is mediated, at least in part, by the transmigration of activated RASFs.
Subfields: Immunology and Allergy, Radiology, Nuclear Medicine and Imaging, Rheumatology
View Paper: https://www.semanticscholar.org/paper/da14d8ea3ccf8aa77a20e234918b760679bba00f
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In Rheumatology
Citations in the corpus
- Update on the Pathomechanism, Diagnosis, and Treatment Options for Rheumatoid Arthritis (2020, background): “Activated fibroblasts not only produce RANK-L and MMPs directly contributing to local joint damage but also migrate between joints, promoting inflammation at other joints (explaining the symmetrical character of the disease) [100].”