IIT Kanpur study finds new link between immune cells, insulin production and diabetes

Researchers at the Indian Institute of Technology (IIT) Kanpur have discovered how certain immune cells inside the pancreas can switch off insulin release within minutes. The study has identified a previously unknown communication pathway between immune cells and insulin-producing cells, offering a new understanding of how diabetes may develop. The findings could also help researchers explore new ways to protect insulin production in people with obesity and type 2 diabetes.
The research, published in the Journal of Clinical Investigation, was jointly led by Simran Singh and Ashish Kumar, the co-first authors, under the supervision of Dr Sai Prasad Pydi from the Department of Biological Sciences and Bioengineering at IIT Kanpur.
Until now, researchers largely understood that obesity could trigger low-grade inflammation in the pancreas, gradually damaging insulin-producing cells over months and years. However, the new study reveals that immune cells can also directly interfere with insulin release through a much faster process.
The human pancreas contains different types of cells, including beta cells and immune cells called macrophages. Beta cells are responsible for producing and releasing insulin, which helps regulate blood sugar levels. Macrophages, meanwhile, help maintain tissue health and balance the immune system.
The IIT Kanpur study found that macrophages can directly communicate with neighbouring beta cells and reduce their ability to release insulin.
“We discovered that immune cells that are present next to beta cells can switch off insulin release within minutes,” said Dr Sai Prasad Pydi.
According to the researchers, this process does not involve the traditional inflammatory signals that scientists have studied for decades. Instead, immune cells send instructions that interfere with the insulin release process.
The researchers identified fats called sphingolipids as the messengers responsible for this communication.
When a particular signalling pathway is activated inside macrophages, these immune cells rapidly release sphingolipids. The neighbouring beta cells then absorb these fats through a transporter present on their surface.
Once inside the beta cells, these fats interfere with the internal machinery responsible for insulin release.
The team traced the process to a receptor called GPR18, which is present on macrophages and triggers the signalling pathway.
Using a precision genetic technique, the researchers switched the signalling pathway on and off inside immune cells. Activating it reduced insulin release in mouse models, while switching it off improved insulin secretion.