Lefèvre, S; Knedla, A; Tennie, C; Kampmann, A; Wunrau, C; Dinser, R; Korb, A; Schnäker, E M; Tarner, I H; Robbins, P D; Evans, C H; Stürz, H; Steinmeyer, J; Gay, S; Schölmerich, J; Pap, T; Müller-Ladner, U; Neumann, E (2009). Synovial fibroblasts spread rheumatoid arthritis to unaffected joints. Nature Medicine, 15(12):1414-1420.
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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.
|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > Center for Integrative Human Physiology
04 Faculty of Medicine > University Hospital Zurich > Rheumatology Clinic and Institute of Physical Medicine
|DDC:||570 Life sciences; biology
610 Medicine & health
|Deposited On:||03 Mar 2010 14:53|
|Last Modified:||27 Nov 2013 18:06|
|Publisher:||Nature Publishing Group|
|Free access at:||Publisher DOI. An embargo period may apply.|
|Citations:||Web of Science®. Times Cited: 115|
Scopus®. Citation Count: 122
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