For the first time, scientists have shown that a protein known as CD36 on the surface of some immune cells is crucial for clearing myelin debris and suppressing nerve cell inflammation in disorders such as multiple sclerosis (MS), according to a new study.
Based on these findings, the researchers suggested that “targeting CD36 holds therapeutic promise for demyelinating disorders such as MS.”
The study, “CD36-mediated uptake of myelin debris by macrophages and microglia reduces neuroinflammation,” was published in the Journal of Neuroinflammation.
MS is an autoimmune disease in which the immune system mistakenly attacks myelin, the fatty protective coating that covers nerve fibers. A hallmark of MS is the abundance of phagocytes (a type of white blood cell) that contain fragments of myelin in active lesions. Phagocytes represent a group of immune cells that normally protect the body by engulfing (eating) harmful invaders such as bacteria.
While the uptake of myelin by phagocytes was initially thought to underlie the degradation of myelin, recent evidence has indicated that clearing myelin debris by phagocytes is also necessary for the repair of the central nervous system (consisting of the brain and spinal cord).
A protein receptor on the surface of phagocytes, called CD36, plays an essential role in the uptake of fatty substances (fatty acids) into cells. CD36 deficiency in mice and humans has been shown to decrease fatty acid uptake in muscle and fat cells.
However, how CD36 is involved in the uptake of fatty myelin by phagocytes, and its role in MS, remains unclear.
To better understand the function of CD36, a team led by researchers at the Hasselt University, in Belgium, conducted a study using cell-based tests as well as a mouse model with MS-like autoimmunity called the experimental autoimmune encephalomyelitis (EAE) model.
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