Fibrocytes in rheumatoid arthritis. New therapy for arthritis. (9)
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One of your immunology research areas is autoimmune disease. We have already discussed rheumatoid arthritis and multiple sclerosis. You discovered a role of circulating cells, fibrocytes, in inflammation and autoimmune disease causation. How could this knowledge be used to treat autoimmune diseases better? That’s a very good question also. What we know about something like rheumatoid arthritis is this. It’s a disease which affects the joints and it’s the progressive disease. It goes from joint to joint. Rheumatoid arthritis is quite distinct from something like osteoarthritis. Osteoarthritis usually targets just one joint – the knee or the hip. Oasteoarthritis is a consequence of overuse, usually from an athletic injury or just aging. Rheumatoid arthritis is progressive. So it may start in one joint. But rheumatoid arthritis will move from one joint to the other. So the big question has always been this. What’s the trigger for rheumatoid arthritis? How is the disease able to move from joint to joint? So a number of years ago we did a very unbiased research. We looked for what circulating cells might be activated in rheumatoid arthritis. We found a number of different circulating cells. Some cells were known. And then we found one very novel cell that nobody had considered in the past. It is called a fibrocyte. As you mentioned this was in patients with rheumatoid arthritis. We found that fibrocytes were activated. If a cell is activated, it tends to suggest this cell is involved in disease in some way. We then went back to small animal models of arthritis. We’re able to show this. Long before there were any symptoms of rheumatoid arthritis in the joints of these small animals. These fibrocytes were already circulating. Fibrocytes increased in numbers and were activated. Indeed we were able to show that fibrocytes moved into the joints. They seemed to participate in the inflammatory response. We then went back to rheumatoid arthritis patients. We looked at those patients that had flares (active disease). Patients that respond to drugs and patients who don’t respond to drugs. We saw good correlations with active rheumatoid arthritis disease. Active fibrocytes reduce in numbers in patients and remission. So the next stage would obviously be to see whether this is true. If you removed those fibrocytes from the blood circulation in patients with a flare (exacerbation). Will that limit rheumatoid arthritis disease? Those clinical trials are all under consideration.