Lowering levels of a protein called reelin — which regulates how permeable blood vessels are to immune cells — reduced infiltration of these cells into the central nervous system (CNS), preventing neuroinflammation and disease progression in a mouse model of multiple sclerosis (MS).
These data, which also showed that Reelin is present at higher-than-normal levels in MS patients during relapses, support Reelin as a potential new therapeutic target for MS. Nevertheless, further studies are needed to confirm the potential benefits of this approach in MS and other inflammation-related conditions, the researchers noted.
“We think we can use this intervention for a wide range of inflammatory diseases that have been difficult to therapeutically address,” Joachim Herz, MD, the study’s senior author, said in a University of Texas Southwestern Medical Center (UTSW)’s press release.
The study, “Reelin depletion protects against autoimmune encephalomyelitis by decreasing vascular adhesion of leukocytes,” was published in the journal Science Translational Medicine.
In MS, circulating immune cells infiltrate the CNS (the brain and spinal cord), where they wrongly attack myelin, the protective sheath that covers nerve fibers, and promote inflammatory reactions that eventually cause nerve cells to die.
Various therapies for MS, approved or in development, aim to prevent immune cells from infiltrating the CNS so to halt neuroinflammation, demyelination (loss of myelin), and disease progression.
However, serious side effects are known with most of these approved therapies, highlighting a need for better and safer immunomodulatory approaches.
Researchers at the UTSW, along with a colleague at Reelin Therapeutics, identified a potentially safer way of preventing immune cell infiltration in MS by targeting a protein called reelin.
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