According to the latest medical discovery a protein that acts as a “master switch” has been found to determine whether certain white blood cells will boost or dampen inflammation. This may open new avenues in rheumatoid arthritis research. Rheumatoid arthritis or RA is an inflammatory disease that causes severe progressive crippling of the joints.
At present patients of RA are treated with a class of drugs known as tumor necrosis factor (TNF) inhibitors. But around one third of them do not respond to these drugs. This study from the Imperial College in London found that a protein called IRF5 acts as a molecular switch that controls whether certain white blood cells, known as macrophages, will promote or inhibit inflammation. The study appeared in the journal Nature Immunology on Sunday.
Authors write that blocking the production of IRF5 in macrophages might be an effective way of treating a wide range of autoimmune diseases, such as rheumatoid arthritis, inflammatory bowel disease, lupus and multiple sclerosis. They also suggest that boosting IRF5 levels might help treat people whose immune systems are weak, compromised or damaged.
Irina Udalova, senior researcher on the study said, “Our results show that IRF5 is the master switch in a key set of immune cells, which determines the profile of genes that get turned on in those cells… This is really exciting because it means that if we can design molecules that interfere with IRF5 function, it could give us new anti-inflammatory treatments for a wide variety of conditions.” The switch according to the team may lie within the genes. The protein may interact with the DNA directly, or act by interacting with other proteins that control which genes are switched on. The researchers are now studying how IRF5 works at a molecular level and which other proteins it interacts with so that they can design ways to block its effects.