Inflammation Hijacks Myelin Repair Cells to Promote Immune Attacks, Study Shows

Inflammation Hijacks Myelin Repair Cells to Promote Immune Attacks, Study Shows

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.

Concepts Keywords
Antigen Oligodendrocyte
Antigen Presentation Oligodendrocyte progenitor cell
Antigen Presenting Cells Multiple sclerosis
Antigens Immune system
Brain Remyelination
Brain Damage Demyelinating disease
CD8 Neurology
Central Nervous System Myelin
Cytotoxic Organ systems
Demyelination Glial cells
Hijacks Nervous system
IFN Gamma Lesion site
Immune System Chronic inflammation
Inadequate Immune infections
Inflammation Brain inflammation
Lesion MS
Molecule Inflammatory immune processes
Myelin Branches of biology
Myelin Sheath
Nature Communications
Nerve Cells
T Cell
T Cells
Tissue Death


Type Source Name
disease MESH infections
pathway BSID Release
disease MESH Inflammation
disease MESH Brain inflammation
disease MESH multiple sclerosis
disease DOID multiple sclerosis
disease MESH demyelination
pathway BSID Immune System
disease MESH development
disease MESH death

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