Publication date: Sep 09, 2019
In people with MS, the body’s own immune system mistakenly recognizes myelin as a foreign molecule and attacks it, causing inflammation and damage to brain nerve cells. Getting OPCs to the site would promote myelin sheath repair, and halt or delay brain damage associated with MS. However, researchers at Johns Hopkins School of Medicine and collaborators have now discovered that pro-inflammatory signals in those injury sites are preventing the OPCs’ maturation into myelin-producing cells – and instead turning them into immune-like cells propagating the attacks against myelin. Using a mouse model of MS, researchers found that introducing T-cells – a type of immune cell involved in the recognition and fight against foreign molecules – that are prone to react against myelin reduced the numbers of OPCs and oligodendrocytes in the brain. These effects were dependent on the T-cells’ production of IFN-gamma, a pro-inflammatory molecule associated with the development of MS. Further studies explained the mechanisms behind the association between IFN-gamma, death of OPCs, and impaired myelin repair associated with MS. Researchers found that IFN-gamma promoted an increase in the activity of several genes associated with specific immune functions in OPCs.