Publication date: Oct 10, 2019
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. 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. Researchers at University of Virginia School of Medicine (UVA) now have discovered that OPCs’ antigen presentation -behavior” in MS is dependent of LRP1, a protein located in their cell membrane. First, the team confirmed the presence of LRP1 in OPCs in healthy human and mouse brains, and in two mouse models of MS associated with extensive myelin loss and induction of immune responses – the experimental autoimmune encephalomyelitis (EAE) model, and the cuprizone model (in which myelin loss is induced by the toxic agent cuprizone). The team proposed that the process of antigen -digestion” (including of myelin in MS) in OPCs is dependent of LRP1, and that these antigens are presented to CD8+ cells during myelin loss in MS, promoting further immune attacks against them.