A recently identified gene allows immune cells to start the self-destructive processes thought to underlie autoimmune diseases such as multiple sclerosis (MS) and rheumatoid arthritis, researchers at Washington University School of Medicine in St. Louis have found.
Researchers showed that mice without the Batf gene lacked a type of inflammatory immune cell and were resistant to a procedure that normally induces an autoimmune condition similar to human MS. They plan to look for other genes and proteins influenced by Batf that could be targets for new treatments for autoimmune diseases.
"Batf allows immune cells to head down a pathway that's been a very hot topic in immunology because of its potential links to autoimmune disease," says senior author Kenneth Murphy, M.D., Ph.D., professor of pathology and immunology and a Howard Hughes Medical Institute investigator. "We showed that Batf regulates the only other gene previously revealed to control this pathway, so Batf may have quite a bit to teach us about autoimmunity."
The findings appear in Nature on July 16.
Lead author Barbara Schraml, Ph.D., found that the loss of Batf affected immune cells known as T cells. Normally T cells take on specialized roles, becoming cells that promote various defensive responses or that recruit inflammatory cells to sites of infection. In mice without Batf, though, one of those roles was blocked: the mice had no inflammatory Th17 cells.
Researchers including Murphy first identified the Th17 pathway four years ago. While such cells help defend the body from bacterial infections, scientists have found that IL17, an inflammatory compound made by Th17 cells, is frequently present at sites of active autoimmune disease.