New study describes molecular process that causes type 1 diabetes

A team of scientists from the Garvan Institute of Medical Research has identified a group of previously unknown immune system cells that may play a major role in the development of type 1 diabetes. The researchers believe that their findings could lead to the creation of new medications to suppress these cells and help individuals avoid the condition.

Type 1 diabetes is an autoimmune disorder that occurs when a person's own immune system attacks and destroys insulin-producing cells in the pancreas. Scientists had previously identified a group of immune cells that were involved in the process but had been unable to develop a complete understanding of how their interactions caused the metabolic disorder.

The new findings, which were published in the journal Immunity, may help improve the medical community's understanding of this process. The researchers showed that a previously unknown subset of CD4+ T cells produce proteins called chemokine receptor 9 (CCR9) and interleukin 21 (IL-21).



Both of these proteins have been shown to play active roles in the ability of another type of immune cell known as CD8+ to cause inflammation, specifically in tissues of the gastrointestinal tract. When pancreatic tissue becomes inflamed, insulin-producing islet cells are killed, resulting in type 1 diabetes.



Some of these cells and their byproducts were previously known to be present in the pancreases of type 1 diabetics. However, their specific modes of operation were poorly understood. The researchers said that by describing the cells' actions in greater detail, it may be possible to develop more effective medications that prevent the destruction of islet cells and onset of type 1 diabetes.

"Recent studies have demonstrated that IL-21 is critical for the maintenance of CD8+ T cells during chronic infection," said Cecile King, who led the investigation. "In our study we showed that IL-21 is also important for the survival of diabetogenic CD8+ T cells."
 
Last updated on
First published on
SHOW MAIN MENU
SHOW SUB MENU