German scientists find that blocking a molecule in the immune system could prevent autoimmune conditions such as type 1 diabetes.
In this new study, published in the journal PNAS, researchers at the Helmholtz Zentrum München report that a mechanism in the immune system prepares for attacks on pancreatic beta cells.
After blocking this mechanism, the researchers are now working on developing treatments that could stop the onset of type 1 diabetes.
A study team led by Dr Carolin Daniel found that children with early signs of immune attack had an increased number of T follicular helper cells (TFH). These are known to be involved in the autoimmune attacks by assisting in the production of autoantibodies against the insulin-producing beta cells.
Upon investigating the mechanisms behind this, the researchers discovered a previously unknown signalling pathway involving a molecule called miRNA92a.
The miRNA92a molecule was found to instigate a complex process that increased proliferation of TFH cells. Particularly, the molecule interfered with the formation of KLF2 and PTEN, two signalling proteins.
To address this, Daniel’s team conducted a series of tests on mouse models of type 1 diabetes. They eventually found that targeting miR92a with a drug called antagonir significantly lowered attacks on pancreatic beta cells.
Moreover, the treatment increased production of regulator T (Treg) cells, which protect the beta cells.
“The targeted inhibition of miRNA92a or the downstream signalling pathway could open up new possibilities for the prevention of type 1 diabetes,” said Professor Anette-Gabriele Ziegler, Institute of Diabetes Research (IDF) of Helmholtz Zentrum München.
Ziegler added that insulin-specific TFH cells could be used as biomarkers to assess the efficacy of treatment success in insulin vaccinations.

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