When things are working normally, your pancreas produces insulin and releases it to regulate the amount of sugar in the blood. Pancreatic beta cells are the only cells in the body that make insulin, but in Type 1 diabetes, those beta cells are damaged and destroyed by the immune system. That’s been understood for decades now, but we didn’t understand why the immune system attacks them. That’s the question Dr. Jason Collier, Director of Islet Biology at Pennington Biomedical Research Center, is answering.
“So what we did was took beta cells and put them under the same conditions that they might be in right before someone became diabetic, and then asked, do they make specific molecules that allow them to talk to the immune system? And if so, what do those molecules do?,” Collier explained.
What he discovered was that the beta cells produce and release a protein into the blood called chemokines.
“Beta cell releases it and it goes into the blood, just like insulin would. And when the immune cells see that protein, it moves towards it. It see’s it as a signal for ‘something’s wrong and I need to go fix it,” Collier said.
So when the immune system arrives, those beta cells are damaged and killed.
Collier describes it like a hail storm. Imagine your car is one of these beta cells, looking and running great. Now imagine that car in a parking lot, during a hail storm. When the beta cells are attacked by the immune system, they come out looking just as bad are your car would -- they are bigger, swollen, and aren’t able to release insulin sufficiently.
Now that we know these proteins trigger the immune system, Collier is asking if there’s a way to turn them off.
“And can you design a drug that shuts this process off and essentially makes the hail storm go away?”
He’s wondering if this trigger for the bombardment by the immune system happens in Type 2 diabetes, linked to obesity.
“We think that’s a possibility”
If the beta cells are protected, then diabetes can be avoided.
“It’d be like flipping off the light switch,” he said.