Research on mice has found evidence of a genetic cause of rheumatoid arthritis and could open the door to development of a new line of drugs.
Research on mice has found evidence of a genetic cause of rheumatoid arthritis (RA). The finding, published online this week in Nature Genetics, could open the door to the development of a new line of drugs to treat RA.
Researchers developed mice with myeloid cells that were incapable of producing the A20 gene and found that the rodents had elevated levels of pro-inflammatory cytokines in their blood and joints and developed RA with severe inflammation. A20 is an intracellular negative regulator of the NF-kB transcription factor, which plays an important role in generating inflammatory response. Excessive activation of NF-kB can lead to a range of inflammatory diseases, including RA.
The arthritis in mice deficient in A20 was not dependent on TNF, a cytokine that usually plays a key role in inflammatory diseases such as RA. This is an important finding, since anti-TNF treatment fails to work in about 30% of RA patients. It is possible that drugs targeting A20 could work in such cases.