A newly-discovered molecule may be capable of speeding up clinical trials to address autoimmune diseases, such as type 1 diabetes.
This is according to a new study, published in EMBO Molecular Medicine. The study suggests that the new molecule, called insulin-like growth factor (IGF-1), could have a direct effect on the failings of immune cells.
Autoimmune diseases are caused by pro-inflammatory T-effector cells (a group of immune cells) erroneously identifying other cells as foreign bodies to be destroyed. The T-effector cells then try to destroy the cells in the same way they try to destroy bacteria. This is allowed to happen because another immune cell, known as the T-reg, also fails. T-reg cells are supposed to control T-effector cells, but fail to shut them down when they are not needed.
The study was conducted by simulating the conditions of type 1 diabetes and multiple sclerosis. The researchers suppressed the symptoms of the diseases by administering IGF-1, which forced the creation of T-reg cells.
The new study discovered that IGF-1 works on T-reg cells directly, instead of acting on another factor that indirectly triggers the production of T-reg cells.
“IGF-1 is already an approved therapeutic and has been tested in many different settings. That means it will be much easier to start clinical trials for IGF-1 in autoimmune and inflammatory diseases than it would if we were proposing a new, untested drug,” said Professor Nadia Rosenthal, Scientific Head of EMBL Australia, and lead author of the study.

Get our free newsletters

Stay up to date with the latest news, research and breakthroughs.

You May Also Like

Twice daily dairy intakes could reduce type 2 diabetes risk

Eating cheese, yoghurt or eggs twice a day could help lower the…

Type 2 diabetes found to be a ‘significant risk factor’ among stroke victims

More evidence has been published which supports that diabetes is a “significant…

Public Health England considers low carb approach for type 2 diabetes

The low carb approach is being considered by the government to be…