Aug. 16, 2011 Researchers from VIB (Flanders Institute for
Biotechnology) and Ghent University have shown that a defective
gene can contribute to the onset of rheumatoid arthritis, an
often-crippling inflammation of the joints that afflicts about
1% of the world's population. Until now, the underlying
molecular mechanism of the disease was largely unclear. In the
study, published in Nature Genetics, the researchers demonstrate
that a cell-specific defect in the expression of the A20 gene
(TNFAIP3) can contribute to the development of rheumatoid
arthritis in mice, thereby identifying A20 as a possible target
for the generation of new drugs. Rheumatoid arthritis (RA) RA is
a chronic progressive joint disease that starts with the
inflammation of the synovial membrane and soft tissues around
the joints, but often spreads to cartilage and bones. The
disease is very painful for the patient. Although the cause of
rheumatoid arthritis remains unknown, autoimmunity plays a
crucial role. Currently, the progression of t