DcR3, a TNF receptor, is one pathologic factor that induces hyperplasia of rheumatoid synovium.
Decoy receptor 3 (DcR3), a tumor necrosis factor (TNF) receptor, actually protects rheumatoid synovial cells from apoptosis, according to researchers at the Kobe University School of Medicine in Japan. Synovial cells initiate the process of rheumatoid arthritis (RA) by provoking cartilage and bone destruction.
The scientists isolated and cultured fibroblast-like synoviocytes (FLS) from 19 patients with RA and 14 patients with osteoarthritis (OA). Expression of DcR3 in FLS was measured and then apoptosis was induced by Fas, a protein ligand and member of the TNF family, and measured. FLS were also incubated with the proinflammatory TNF-alpha prior to Fas-induced apoptosis.
DcR3 was expressed in both the RA and OA FLS, with no significant quantitative differences between the samples. However, TNF-alpha increased DcR3 expression and inhibited Fas-induced apoptosis in RA FLS but not in OA FLS.
“We believe that DcR3 expressed in RA FLS is increased by TNFa, making it one of the pathologic factors that induces hyperplasia of rheumatoid synovium,” states the author of the study, Yasushi Miura, M.D., Ph.D. “Thus, strategies aimed at down-regulation of DcR3 in FLS warrant further investigation as a possible therapeutic approach in RA.”
Since DcR3 is overexpressed in tumor cells, including lung and colon cancers, gastrointestinal tract tumors, and leukemia, this research identifies DcR3 as a potential target for cancer as well as RA, according to the team.
The results of the study are published in the April 2007 issue of Arthritis & Rheumatism.