No T Cells Allowed: Guarding Against RA

Arthritic inflammation may be prevented by new treatment target

March 8, 2012 / Author:  / Reviewed by: Joseph V. Madia, MD

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(dailyRx News) Treatments for rheumatoid arthritis come in two forms: treatments that deal with symptoms and those that attack the disease itself. Now, scientists may discovered a new target for that second type of treatment.

Researchers may have found a new way to treat rheumatoid arthritis by stopping T cells (the white blood cells that cause inflammation and joint damage) from entering the joints.

"Ask your doctor about treatments for rheumatoid arthritis."

Rheumatoid arthritis is a type of autoimmune disease, meaning that the body's own immune system mistakenly attacks healthy joints.

Treatment for rheumatoid arthritis often involves blocking the signals that lead to the autoimmune attack on the joints. This new method, on the other hand, stops damage by keeping the T cells from entering the joints altogether.

Dr. Graeme O'Boyle, of Newcastle University in the United Kingdom, explains how this new treatment method works: “Imagine that the damaged joint is covered in flags which are signalling to the white blood cells. Traditional treatments have involved pulling down the flags one by one but what we have done is use an agent which in effect ‘blindfolds’ the white blood cells. Therefore, they don’t know which way to travel and so won’t add to the damage.”

From their study, Dr. O'Boyle and colleagues found that an agent called PS372424 stops T cells from moving toward arthritic joints.

PS372424 attaches itself to a certain receptor called CXCR3. Because CXCR3 is only found on activated T Cells, the PS372424 agent only 'blindfolds' these T cells while leaving other white blood cells to go about their business.

Some rheumatoid arthritis treatments are not as specific as this new method may be. While they can block the activated T cells from attacking joints, they can also block otherwise healthy white blood cells. These drugs can do damage to a patient's immune system.

According to Dr. O'Boyle, "By desensitizing damaging white blood cells using CXCR3 they are not directed to migrate towards rheumatoid sites."

"The advantage of this system is that it is much more specific than current medications and may not compromise the immune system," he explains.

Professor Alan Silman, medical director of Arthritis Research UK, the organization that funded the study, says, "Although modern treatments have changed the outcome for many patients with rheumatoid arthritis, firstly not all patients respond to them and secondly, even in those patients who do respond in some way, we can't completely get rid of the inflammation that damages their joints."

While this study may seem promising, one must keep in mind that the findings come from a mouse-model of arthritis. More work needs to be done before this treatment target is tested in humans.

"This research is very exciting, as although it is in its early stages, if it can be transferred to humans it could shut down the inflammation that causes rheumatoid arthritis," Professor Silman explains.

The results of this research are published in the Proceedings of the National Academy of Sciences.