An immune system component that is a primary cause of bone destruction and inflammation in autoimmune diseases actually protects bone in the oral cavity from infectious pathogens, according to researchers at the University at Buffalo (UB).
The component, IL-17 or TH-17, was recognized only in the past 18 months. "We know now that almost all autoimmune diseases, at least in the mouse model, are caused by TH-17 cells," says Sarah L. Gaffen, Ph.D., associate professor of oral biology in the UB School of Dental Medicine, associate professor of microbiology and immunology in the UB School of Medicine and Biomedical Sciences, and senior author. Therapies that target IL-17, a protein hormone made by T-helper cells, or its cellular receptor are currently being developed.
Dr. Gaffen and her team, however, have discovered that, in contrast to its action in rheumatoid arthritis (RA), IL-17 actually protects bone in the oral cavity from infectious pathogens such as Porphyromonas gingivalis, a bacterium that plays a major role in most periodontal disease in humans. “This new information,” Dr. Gaffen points out, “has forced scientists to revise completely how they view their favorite disease. Everyone now has to rethink the causative mechanism.”
They conducted the research in mice bred to have no receptors for IL-17. "I predicted these mice without the IL-17 receptor were going to be protected from periodontal bone loss, just like they’re protected from arthritic bone loss," Dr. Gaffen adds. "In fact, we got the opposite result. The mice without IL-17 were much more susceptible to bone loss caused by periodontal disease, compared to normal mice.
"It turns out that IL-17 is really important in regulating neutrophils by causing other cells in the vicinity to recruit these infection fighters to the infection site," Dr. Gaffen explains.
IL-17 would likely be toxic if given systemically, so it may not be a therapeutic candidate to increase immunity, she adds.
The research findings appear in the May issue of Blood.