Inflame on, inflame off? A 'master switch' protein decides

UK scientists have identified a protein in white blood cells that acts as a ‘master switch,’ determining whether to stimulate or suppress inflammation. This finding could lead to new drugs for diseases like rheumatoid arthritis.

When the body’s defense system is faced with infections or tissue damage, inflammatory responses help start the healing process. But excessive inflammation can harm the body; with rheumatoid arthritis, the joints become swollen and painful.

Immune cells called macrophages – ‘big eaters’ because they ingest foreign material – release chemical signals that affect the behavior of other cells.

The new research shows that a protein called IRF5 acts as a molecular switch that controls whether macrophages promote or inhibit inflammation.

The master switch in a key set of immune cells determines the profile of genes that get turned on in those cells, says senior researcher Irina Udalova of the Imperial College London.

Blocking the production of IRF5 in macrophages could provide anti-inflammatory treatments for inflammatory bowel disease and a range of other autoimmune diseases, including lupus and multiple sclerosis.

Or, boosting IRF5 levels might help to treat people whose immune systems are compromised.

"Diseases can affect which genes are switched on and off in particular types of cells,” Udalova says. “Understanding how this switching is regulated is crucial for designing targeted strategies to suppress unwanted cell responses.”

Rheumatoid arthritis is a chronic inflammatory disease affecting around 1% of the world's population. Many patients are treated with a class of drugs known as tumor necrosis factor (TNF) inhibitors. The drugs target TNF, an important signaling chemical released by immune cells to stimulate inflammatory responses, and they’re made by various drug firms, including Abbott Laboratories, Merck & Co, Pfizer and Amgen [Reuters].

But around 30 percent of patients don't respond to anti-TNF drugs.

The study was published in Nature Immunology on Sunday.

Image: NIH

This post was originally published on Smartplanet.com