A study by Researchers at the University of Rochester Medical Center identify that powerful drugs used to treat patients with rheumatoid arthritis have a profound and unrecognised effect on the immune system
It breaks up molecular 'training camps' for rogue cells that play an increasingly recognized role in autoimmune diseases lupus.
The researchers reported that drugs known as anti-TNF compounds - which include drugs such as Enbrel, Humira and Remicade - affect our B cells, which play a role in many autoimmune diseases.
The researchers found that anti-TNF compounds help eliminate abnormal B cell activity in patients, raising the possibility that the drugs improve the health of patients in a way no one has realized before.
"The most important considerations for any drug are: Is it safe, and does it work?" said Ignacio Sanz, M.D., professor of Medicine, Microbiology and Immunology, and one of two rheumatologists leading the research.
"The answer is certainly 'yes' to both questions for these anti-TNF compounds. The drugs have revolutionized the treatment of patients with rheumatoid arthritis. But it also turns out that, even though millions of patients have been treated with these medications, we really haven't understood to a significant degree how they actually work," Sanz added.
Sanz and colleagues found that anti-TNF drugs disrupt the architecture of structures in our lymph system called germinal centers, which are a type of training ground for immune cells.
The team found that the drug inhibit the function and organization of cells known as follicular dendritic cells, which help form the germinal centers.
For the study, the researchers involved 45 patients with rheumatoid arthritis and 22 healthy adults. Some of the patients with arthritis received etanercept (Enbrel); others received an older medication, methotrexate; and others received both.
They found that the anti-TNF medication dropped the percentage of memory B cells in the lymph tissue by about 40 percent in patients.
They also found that arthritis patients who received anti-TNF therapy had about one-quarter the number of germinal centers as other arthritis patients. The germinal centers that did exist in patients were smaller and less organized.
"Follicular dendritic cells are like the fabric that keeps together the germinal centers. If we can disrupt the formation of that network of cells, as anti-TNF compounds do, that should decrease the number of faulty B cells. And that's exactly what we found," said Sanz.
This is one of the first studies to explore how anti-TNF compounds affect B cells in patients with rheumatoid arthritis.
The study is published in the Jan. 15 issue of the Journal of Immunology.