Research finds blocking single receptor can hinder rheumatoid arthritis

September 23, 2014

Topic: physical therapy

Researchers from the University of Illinois have discovered that controlling a certain receptor can actually prevent the development of rheumatoid arthritis.

Researchers from the University of Illinois have discovered that controlling a certain receptor can actually prevent the development of rheumatoid arthritis. The findings were published in the Journal of Immunology.

The receptor is located in cells of the arthritic bones and joints. They hope their findings can offer a new solution for alleviating the condition's detrimental effects.

A common and disabling condition
The American College of Rheumatology stated that rheumatoid arthritis is one of the most disabling types of arthritis. Approximately 1.3 million people have the condition. Rheumatoid arthritis is an autoimmune disease, so people experience a variety of symptoms and pain levels. People most commonly have joint stiffness, pain and inflammation that can limit range of motion. However, there are some treatment methods available. There are medications, such as antirheumatic drugs that can help slow the condition's progression, on the market. Usually these medications are prescribed with an anti-inflammatory drug. Occupational and physical therapy can help increase mobility.

The receptor that the authors of the new study evaluated, known as toll-like receptor 5, or TLR5, is in white blood cells that move from the blood into the affected joint. The receptor is most commonly found in myeloid cells, which sit in the fluids of joints.

Lead researcher Shiva Shahrara and her colleagues discovered in a previous study that activating TLR5 caused abnormal blood vessel development in the joint fluid of people with rheumatoid arthritis. In this study, the researchers discovered that the receptor regulates an inflammation-causing molecule called TNF-alpha. This molecule brings more myeloid cells to the joint, which turns them into bone-destroying cells known as osteoclasts.

Testing reactions
The study authors tested activating the receptor in several ways. When the researchers placed myeloid cells with TLR5 next to the fluid of a joint containing rheumatoid arthritis, the cells floated into the fluid. But when the researchers placed an antibody in the cells' path, the cells could not float in as easily. The researchers suspect that the TLR5 is drawn to something in the joint fluid, such as its binding protein, which may be found in the joints of people with rheumatoid arthritis. The study authors also found that the levels of TNF-alpha were higher around the presence of TLR5 cells.

They believe the pair has a positive correlation. If one increases, so does the other.

"Not only do TLR5 and TNF-alpha regulate each other, but they work synergistically to attract more myeloid cells into the joint, where they are transformed into bone-eroding cells," Shahrara said in a statement.

Looking to the future
The researchers tested their findings on mice. When they gave the mice an antibody that blocked TLR5, the mice had reduced swelling and inflammation in their joints. Shahrara and her colleagues believe the findings could uncover a treatment to help prevent continual joint inflammation and bone erosion in late-stage rheumatoid arthritis.

"The receptor is a major driver of inflammation and bone degradation," Shahrara noted. "Blocking this receptor could have significant therapeutic value in interrupting joint swelling and bone loss in patients with rheumatoid arthritis."

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