Brain inflammation in multiple sclerosis (MS) hijacks immature myelin repair cells, not only preventing myelin restoration but also promoting sustained inflammation and immune attacks against myelin, a preclinical study shows.
The work, funded in part by the National MS Society, highlights immature myelin repair cells and their inflammatory/immune processes as new potential therapeutic targets for MS.
The study, “Oligodendrocyte precursor cells present antigen and are cytotoxic targets in inflammatory demyelination,” was published in the journal Nature Communications.
Nerve fibers are surrounded by a protective myelin sheath that allows electrical signals to be quickly transmitted throughout the body. Upon myelin damage in the brain, immature, stem-like cells called oligodendrocyte precursor cells (OPCs) travel to the lesion site, where they mature into oligodendrocytes — myelin-producing cells capable of restoring the myelin sheath.
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. In addition, the myelin repair process is impaired in people with MS.
Increasing research has focused on the development of therapeutic approaches to recruit OPCs to the sites of myelin damage. 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.
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