A study published in the journal Arthritis and Rheumatology reveals that cartilage plays an active role in the remodeling and destruction of joints observed in rheumatoid arthritis (RA), which is contrary to what was previously thought. Tommy Liu, PhD, Ian Wicks, MB BS, FRACP, PhD, Kate Lawlor, PhD, and Ben Croker, PhD, along with other colleagues from the Walter and Eliza Hall Institute, made the discovery while exploring the role of the protein SOCS3 in controlling inflammation during RA.
Liu says cartilage was thought to be a victim of an overzealous immune system rather than playing an active role in RA. Liu states, “Our study has shown for the first time that cartilage participates in the production of inflammation-signaling chemicals and contributes to its own destruction.”
The study investigated how the molecules, known as suppressors of cytokine signaling (SOCS) molecules, that control the flow of chemical messages within and between cells regulate inflammation in RA, according to a Walter and Eliza Hall Institute news release. When the Melbourne researchers created a model that lacked SOCS3 molecules in the cartilage, they discovered that tissue degradation was increased.
Liu explains, “Without SOCS3, cartilage cells produced enzymes that drove tissue degradation and increased inflammation by releasing signaling molecules that triggered an increased autoimmune response. We also found that cartilage could produce a protein called RANKL that triggers bone remodeling.”
Liu adds, “These results show that cartilage is not an innocent bystander that gets damaged as a result of rheumatoid arthritis, but instead plays an active role in disease progression.” As there is no cure for RA, and few treatments are effective in slowing the onset of the condition, Liu says, “Targeting the action of these inflammatory chemical messages could boost the efficacy of current treatments.”
Photo Appears Courtesy of Walter and Eliza Hall Institute
[Source: Walter and Eliza Hall Institute]