The tonsils and lymphoid tissues in the intestinal tract that help protect the body from external pathogens are the home base of a rare immune cell newly identified by researchers at Washington University School of Medicine in St. Louis.
The researchers indicate that the immune cells could have a therapeutic role in inflammatory bowel diseases (IBD) such as Crohn's disease and ulcerative colitis.
Their report will appear in an upcoming issue of the journal Nature and is currently available through advanced online publication.
"These cells have an anti-inflammatory effect," says the article's lead author Marina Cella, M.D., research associate professor of pathology and immunology. "In the gut, we have beneficial bacteria, and it's important that the body does not recognize them as something detrimental and start an inflammatory reaction, which could ultimately promote tissue damage and inflammatory or autoimmune diseases such as IBD. The cells we've discovered are important for keeping such harmful inflammatory processes in check."
The cells are a type of natural killer (NK) cells, which are white blood cells classically known to eliminate tumor cells and cells infected by viruses. Because of their killer tendencies, NK cells are carefully controlled and don't act until they receive the right signal.
Some of the signals that activate the newly discovered cells are the same signals that turn on a different immune cell with strong inflammatory properties that can promote cell death and tissue damage if chronically active. But the anti-inflammatory cells, termed NK-22 cells, that the Washington University researchers discovered have the opposite effect — they promote cell proliferation and wound healing.
"That finding suggests that these cells play a role in maintaining a balance in the immune system between inflammatory processes and anti-inflammatory processes," says coauthor Jason Mills, M.D., Ph.D., assistant professor of pathology and immunology and of developmental biology. "They make sure that factors that turn up inflammation can be counteracted by the coordinated activation of anti-inflammatory effects."