When the immune system is activated, certain receptors that work as “switches” turn on processes that help the body fight pathogens that cause disease. If these receptors stay switched on after the body has protected itself, the immune system may begin to attack healthy parts of the body.
In a new study, MU scientists have determined that a type of P2 nucleotide receptors, known as a P2Y2 receptor, plays a role in Sjögren’s syndrome, a predominately female disease affecting 4 million Americans. Sjögren’s syndrome is believed to be caused by immune cells attacking and destroying the exocrine glands that produce tears and saliva. Understanding how the P2Y2 receptor interacts with the immune system could lead to novel targets for therapeutic strategies for Sjögren’s syndrome, including engineering salivary gland tissue.
“There is no known cure for Sjögren’s syndrome; patients with the syndrome experience a decrease in their quality of life with few treatment options,” says Gary Weisman, professor of biochemistry and an investigator in the Bond Life Sciences Center. “Although designed to help us, the immune system is the cause of a lot of our grief when it is over-activated. P2Y2 receptors are known to be activated in damaged or diseased salivary glands and may play a role in tissue repair. They can be either the good guy or the bad guy depending on the cell type in which they are located.”
P2 receptors are present in nearly all cells and tissues where they mediate diverse functions, including muscle contraction, neurotransmission, insulin secretion, wound healing and cell growth. Previous studies have indicated that P2Y2 receptors may have a role in several diseases, including cystic fibrosis, cardiovascular disease, Parkinson’s disease and Alzheimer’s disease.