Offering a significant advance in the understanding of rheumatoid arthritis, researchers at Brigham and Women’s Hospital and the Joslin Diabetes Center have found that specialized immune cells may play a role in fostering the painful condition.

The condition, marked by inflammation of the joints, affects 2.1 million Americans and strikes women at a higher rate than men.

The cause of arthritis is unknown, but the researchers found that mast cells—immune cells traditionally known to trigger allergic inflammation—may release inflammatory chemicals in response to arthritis-associated signals.

David M. Lee, a research fellow in medicine at the Brigham’s rheumatology division, collaborated with researchers from the Diabetes Center to publish his findings in the Sept. 6 issue of the journal Science.

The researchers tested strains of mice without mast cells and found they were resistant to arthritis.

But when mast cells were reintroduced to some of these mice, they became susceptible to the ailment.

Although the exact cause of arthritis is unclear, it is known to stem from an immune response in the body.

And mast cells have been known to be receptive to antibodies associated with arthritis.

The new research indicates the possibility that these cells actually play an important role in the onset and development of arthritis.

Lee said he is cautious but optimistic about the therapeutic implications of the discovery.

“We were looking at mouse arthritis, but it does have a lot of similarities to the human disease,” he said. “Working back to the human system will hopefully lead to therapy down the road.”

According to Christophe Benoist, a professor of medicine at the Diabetes Center who collaborated with Lee, this represents the newly recognized potential of mast cell research.

“Mast cells have been unrecognized for a long time, but are now being implicated in many physiological pathways with practical consequences,” he said.

Benoist said the increased attention to mast cells may hold payoffs for a large range of diseases.

He called the discovery “another point from which we can attack autoimmune diseases” such as arthritis.