CORNELL (US) — A cell from the body’s own immune system appears to be responsible for Crohn’s disease, a condition that causes pain and digestive unrest for millions of Americans.
“Auto-immune diseases are on the rise in this country but their causes have remained largely unknown,” says Eric Denkers, professor of immunology at Cornell University.
“It’s possible that these diseases are more common in the West because we’re too clean. Exposure to germs trains immune systems how to respond to threats.”
“Early protection from germs may contribute to the increasing prevalence of immune system overreactions in our population, leading to auto-immune problems like allergies and inflammatory bowel disease.”
“We noticed that the initial intestinal inflammation these parasites can cause looks very similar to what happens during Crohn’s disease,” Denkers says.
Similar symptoms arise when some hosts first face the prevalent protozoan Toxoplasma gondii.
“Our lab has started using Toxoplasma to model Crohn’s disease in humans and help us find the pivotal perpetrator, which has turned out to be a cell from our own immune forces.”
Specialized immune cells called intraepithelial lymphocytes patrol intestinal walls. Upon encountering invaders, they release messenger proteins that call more immune cells to the battleground.
“Too many messenger proteins recruit too many immune cells, causing inflammation that can devastate the host’s own tissue,” Denkers explains. “Bad balance between good bacteria, bad bacteria, and immune interactions like inflammation cause Crohn’s disease.
“For the first time we’ve discovered how infection can turn these immune cells pathogenic, stimulating them to cause disease, inflammation and necrosis in the small intestine.”
“This marks a major leap toward understanding human Crohn’s disease. Unveiling this kind of immunological interplay may lead to improved prevention and care in an array of auto-immune diseases.”
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