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A Newly Identified Immunosuppressive Protein in Rheumatoid Arthritis

re incubated with the proinflammatory TNFá prior to Fas-induced apoptosis, and apoptosis was measured.

DcR3 was expressed in both the RA and OA FLS, with no significant quantitative differences found between the samples. However, TNFá increased DcR3 expression in and inhibited Fas-induced apoptosis in RA FLS, but not in OA FLS.

This study affirms DcR3 as an immunosuppressive agent that actually protects destructive rheumatoid synovial cells against death. "We suggest that DcR3 expressed in RA FLS is increased by TNFá, making it one of the pathologic factors that induces hyperplasia of rheumatoid synovium," states researcher and author, Dr. Yasushi Miura. "Thus, strategies aimed at down-regulation of DcR3 in FLS warrant further investigation as a possible therapeutic approach in RA."

Even in this era of TNF-alpha inhibitors and other powerful drugs, there are constantly new aspects of biology being found that offer different forms of treatments for rheumatoid arthritis.

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