After 20 years of searching, scientists have finally identified the fifth and final molecule that the immune system attacks in order to trigger type 1 diabetes, completing the puzzle and providing new hope for treatments.
Type 1 diabetes is an autoimmune condition, which means it's caused by a patient's own immune system attacking their body - in this case, their insulin-producing beta cells. For years, scientists have struggled to figure out exactly how the immune system attacks, and which targets it aims for, but now it looks like they've finally done it.
"With this new discovery, we have now finished identifying what the immune system is targeting - we have the complete picture," lead researcher Michael Christie from the University of Lincoln in the UK, told James Gallagher over at the BBC.
Now that we know which targets the immune system is gunning for, the hope is that we'll be able to figure out a way to stop this from happening.
Researchers have long been studying the antibodies - the tiny weapons that the immune systems of type 1 diabetics produce against their beta cells - but figuring out the specific, molecular targets of these antibodies is tricky. The team compares it to figuring out someone's identity from their silhouette.
Researchers had previously managed to identify four out of the five targets, but for the past 20 years they've struggled to nail down the fifth one, simply giving it the pseudonym of 'Glima' in the research. (As far as we can tell, that's a fancier alternative to throwing up your hands and saying, "Who knows, let's call it 'molecule X'.")
But now Glima's true identity has been revealed as the protein Tetraspanin-7, and that means we finally have a full understanding of what goes wrong to cause type 1 diabetes.
"We already had some knowledge about the physical properties of Glima, but its molecular identity has for many years proved elusive," said Christie. "This has hampered the development of relevant autoantibody tests, but our research successfully identified Glima as the substance Tetraspanin-7."
So we now know the five molecular targets in type 1 diabetes are:
"Once the immune system decides it wants to get rid of something it's very hard to stop, so diabetes has proved to be a difficult disease to prevent," Christie told the BBC. "So we're hoping that, by having identified the major targets in the disease, we can find ways to prevent it by blocking the immune response to these five proteins without leaving that person vulnerable to infections."
There's a lot of work to be done before this knowledge can be turned into something that could benefit diabetics - for example, an early screening test for type 1 diabetes - and treatments that could potentially stop the condition from developing in the first place.
But according to Diabetes UK, the new research is a big step in the right direction.
"In order to prevent type 1 diabetes, we need to fully understand how the immune response that damages insulin-producing cells develops in the first place," said spokesperson Emily Burns. "We hope that the findings here will be used to improve the identification of those at risk of type 1 diabetes and, in the long term, inform the crucial development of therapies."
"With recent improvements in our understanding of the disease I'm very hopeful we'll develop a treatment now," added Christie. "I have a lot more confidence than even five years ago."
The research has been published in the journal Diabetes.