NIH scientists find a novel mechanism that controls the development of au...( Scientists at the National Institute...),Health

Scientists at the National Institutes of Health (NIH) have found a mechanism in the immune systems of mice that can lead to the development of autoimmune disease when turned off. The findings shed light on the processes that lead to the development of autoimmunity and could also have implications for the development of drugs to increase the immune response in diseases such as cancer and HIV. The study paper appears online today in the journal Nature.

The scientists from the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) and the National Institute of Allergy and Infectious Diseases (NIAID), both part of the NIH, studied immune system T cells specifically the helper T cell, an immune system component that helps other cells fight infection. They focused on the protein furin, an enzyme that plays an important role in the functioning of T cells.

Scientists have been limited in their ability to study the protein furin, because other enzymes can perform some of the same functions. Also, furin is essential to life, so scientists have been unable to create a mouse without furin that lives past the embryo stage of development. Since the NIH scientists were unable to see what a mouse without furin would look like, they collaborated with Belgium scientists to create a mouse without furin only in T cells. What they discovered was that mice without furin in these cells developed systemic autoimmune disease. This means that the immune systems of the mice attacked their own cells and tissues throughout their bodies.

"We already know that furin seems to have roles in a variety of human diseases, such as cancer, cystic fibrosis and infectious diseases," says lead author Marko Pesu, Ph.D., in the NIAMS' Molecular Immunology and Inflammation Branch. "These findings show that having no furin in certain immune system cells can increase the immune response and lead to autoimmune disease in mice."

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