IBRI IN THE NEWS: How autoimmunity starts

September 01, 2021

New research indicates body organs under stress may attract attackers from the immune system

When Decio Eizirik began treating patients with type 1 diabetes in the 1980s, he was pretty sure about what was behind the disease: an immune system gone haywire. People with the illness lacked insulin, a crucial hormone, because beta cells in the pancreas - the body's insulin factories - were being attacked and destroyed by immune system cells. "At that time, the idea was that if you could control the immune system, perhaps you could prevent diabetes," says the endocrinologist, who now has research appointments at the Indiana Biosciences Research Institute and at the Free University of Brussels in Belgium. (He no longer sees patients.)

This was the classic model of an autoimmune disorder: protector cells that turn on their bodily kin. Although treatments with extra insulin could keep people with diabetes alive, the immune assault on innocent beta cells was the root of the problem. "People saw beta cells as being like the corpse at a funeral: it's the focus of a lot of attention, but it's doing nothing," Eizirik recalls.

Now, however, those beta cells are not looking quite as innocent, and the immune system is looking like it has gotten an unfair share of blame. Over the course of several decades Eizirik - and a number of other researchers - has become convinced that beta cells can actually trigger the disease. The way beta cells do this began to emerge in the late 1990s, when Eizirik measured levels of chemical signals from the cells in the pancreas. Those experiments showed that in certain circumstances the cells produce their own inflammatory chemicals, which act as flares that draw the attention, and ire, of immune system cells.

To read the full article, go to Scientific American (paid subscription).