The discovery of a new type of immune cell could help block autoimmune diseases such as type 1 diabetes, a new study finds.
Researchers at The Scripps Research Institute (TSRI) have discovered cells which resemble conventional T cells, but can transform into T regulatory cells (Tregs).
Treg cells are known to be able to control the body’s immune response and protect the body from autoimmune disease. Separate clinical trials are currently investigating how Treg cells can enter the pancreas, and Scripps scientists will now try to use these new cells to control diseases such as type 1 diabetes.
In this new study, researchers isolated an individual Treg from a mouse model of type 1 diabetes. They then inserted its nucleus – which contained the unique genetic immune receptor information – into a mouse egg that had its own nucleus removed.

This cloning method is known as Somatic Cell Nuclear Transfer (SCNT) and led to the creation of a mouse that produced only the original Treg.
The researchers discovered that the new mouse’s Treg cell originated in a lymphoid organ called the thymus. This made it a ‘naturally’ arising Treg, called an nTreg. These cells are distinct from those that develop outside of the thymus, which are known as peripherally-induced Tregs (pTregs).
The study team then observed a second type of T cell in the thymus and spleen. This cell appeared different to the nTreg, but it was genetically identical, and turned out to be a precursor for the nTreg.
Senior study author and TSRI biologist Oktay Kirak explained: “We realised that the one T cell type exists in two functional states. That was a huge surprise – I didn’t believe it at first.
“This study was eye-opening. You wouldn’t expect these cells to have this ability. The best analogy I have is Clark Kent turning into Superman. Clark Kent looks like an Average Joe, so no-one would expect him to have the same abilities as Superman.”
The cells had different appearances because of a gene called Fox93, which was inactive in the pTreg, but can transform the cell into an nTreg once activated.
The researchers believe pTregs – which are known to be present in people with type 1 diabetes – could be activated in response to immune challenges, such as cancer and autoimmune diseases, but still cannot prevent an autoimmune attack.
“Whatever they are doing there, it is not sufficient to stop the autoimmune attack”, said Kirak, whose team is now planning to develop markets to identify different Treg and pTreg cell types.
The findings appear in the journal Proceedings of the National Academy of Sciences.

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