Blocking production of the low-density lipoprotein receptor-related protein 1 (LRP1) — involved in inflammatory and immune responses — specifically in myelin repair cells halts neuroinflammation and promotes myelin repair, a preclinical study shows.
These results, from two mouse models of multiple sclerosis (MS), shed light on the underlying mechanisms by which myelin repair cells contribute to myelin loss and cell damage upon neuroinflammation, and pinpoint LRP1-associated pathways as new potential therapeutic targets.
The study, “The active contribution of OPCs to neuroinflammation is mediated by LRP1,” was published in the journal Acta Neuropathologica.
In people with MS, the body’s immune system mistakenly recognizes myelin — the protective sheath around nerve fibers — as a foreign molecule and attacks it, causing inflammation and damage to brain nerve cells.
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.
However, the myelin repair process is impaired in people with MS. Increasing evidence highlights that OPCs — once thought to have only a beneficial role in the process of myelin repair — play an active role in MS-associated myelin loss.
A previous study has shown that neuroinflammation hijacks OPCs not only to prevent their differentiation into myelin-producing cells, but also to promote further inflammation and immune attacks against myelin.
Researchers found that in an MS environment, OPCs acted like some immune cells, “ingesting” myelin molecules and presenting them to a specific type of immune T-cell known as CD8+ cells to induce immune reactions against them — a process called antigen presentation.
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