Cytokine found to control trigger of inflammatory bowel disease

April 18 (UPI) -- A study by Georgia State University found that a certain cytokine can control whether immune cells promote or suppress inflammatory bowel disease.

Cytokines are small proteins that help cells communicate during immune responses.

Researchers identified a specific cytokine that they believe is responsible for whether immune cells promote or suppress inflammatory bowel disease, which could lead to new treatments.

Nearly 1.5 million Americans have some sort of inflammatory bowel disease, a chronic inflammation of all or part of the digestive tract. There are two main types of inflammatory bowel disease, Crohn's disease and ulcerative colitis, which both can cause severe diarrhea, pain, fatigue, weight loss and death.

Researchers from Georgia State collaborated with researchers from Emory University and the University of Michigan to find that cytokine IL-36y controls whether T cells become aggressive or suppressive in mouse models.

The team found IL-36y promoted the development of a specific type of T helper cell, Th9, which is associated with several diseases like asthma, cancer and inflammatory bowel disease.

"We were very intrigued whether the cytokine we were studying, IL-36y, could be promoting intestinal inflammation through the development of these Th9 cells, and that's in fact what we found," Dr. Tim Denning, associate professor in the Institute for Biomedical Sciences at Georgia State, said in a press release.

"When we were discovering this, we also found it simultaneously inhibits a suppressive population of T cells termed regulatory T cells or Tregs, which are known to suppress inflammatory bowel disease. Our conclusions were that IL-36y plays a critical role in driving the differentiation of pro-inflammatory Th9 cells and inhibiting the development of the suppressive Tregs. We think this can have major implications in the treatment of human inflammatory bowel disease, particularly ulcerative colitis, which has been shown to be associated with Th9 cells."

The study was published in Mucosal Immunology.