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Researchers of the
Australian National University (ANU) have identified why certain cells in the body, known as Th17 cells, become rogue and promote the onset of autoimmune diseases such as multiple sclerosis (MS).
In a new study published in
«Nature Communications», scientists discovered a previously unknown and unpleasant side effect of a bacteria-fighting weapon in the entire immune system, neutrophil extracellular traps (NETs).
NETs are responsible for directly enhancing the production of harmful Th17 cells.
“This discovery provides a new therapeutic target to interrupt these damaging inflammatory responses,” said lead author Alicia Wilson of the
Johannes Gutenberg University of Mainz (Germany).
The researcher points out that the information opens “the doors to the development of new therapies targeting this harmful NET-Th17 interaction, with the hope of improving treatments for MS and other autoimmune diseases in the future.”
Similar in appearance and function to spider webs, NETs are produced by a subset of white blood cells called neutrophils. They capture and kill nasty bacteria and are designed to protect the body from infection.. But as the Australian researchers show, NETs also have a “dark side” that causes them to manipulate Th17 cells, making them stronger and more dangerous.
Th17 cells are normally beneficial because they defend the body once morest bacterial and fungal infections, but when they become overactive, they can cause serious inflammation. In their aggressive form, Th17 cells are responsible for promoting autoimmune diseases such as MS.
“We found that NETs cause Th17 cells to become more powerful, which increases their detrimental effects,” said lead author Anne Bruestle.
By understanding how NETs turn Th17 cells from friend to foe, scientists believe they can use targeted therapies to inhibit the negative effects of NETs.
Bruestle and a team of international researchers believe that a drug originally designed to treat sepsis might be used to target bad Th17 cells and, in turn, help MS patients better manage their condition by providing relief.
The drug was developed by Professor Christopher Parish and his team, also from ANU.
“Since we see in both mice and humans that a group of proteins in NETs called histones can activate Th17 cells and cause them to become harmful, it makes sense that our histone-neutralizing drug, mCBS, which was developed to treat sepsis , may also be able to inhibit the undesirable effects of NETs that are related to driving MS,” said Professor Parish.
“While we can’t prevent autoimmune diseases like MS, with these kinds of therapies we hope to treat the condition and make it more manageable for people living with MS,” Bruestle concludes.
