Multiple Sclerosis | Why Does the Immune System Attack Its Own Nerves?

In the central nervous system, which includes the brain and spinal cord, nerve fibers are wrapped in a protective, insulating layer called the myelin sheath. This fatty substance is crucial for the rapid and efficient transmission of electrical signals, or nerve impulses, between nerve cells. Think of it as the plastic insulation around an electrical wire; it prevents the signal from dissipating and allows it to travel quickly to its destination. In multiple sclerosis (MS), the body's own immune system mistakenly identifies myelin as a foreign invader. Specialized immune cells, primarily T-cells, cross the blood-brain barrier—a protective filter that usually keeps harmful substances out of the brain. Once inside the central nervous system, these cells trigger an inflammatory response. They release chemicals that damage the myelin and the cells that produce it, which are called oligodendrocytes. This process of destroying myelin is known as demyelination. As the myelin is stripped away, it leaves behind hardened scar tissue, referred to as sclerosis or lesions. This damage disrupts the communication pathway of the nerves, leading to the neurological symptoms characteristic of MS.

The loss of myelin has profound effects on nerve function. When the myelin sheath is damaged or destroyed, the transmission of nerve signals along the axon is impaired. The electrical impulses may slow down, become distorted, or stop altogether. The specific symptoms a person with MS experiences are directly related to the location of the demyelination within the central nervous system. For example, if lesions form on the optic nerve, it can lead to vision problems like blurred vision or pain with eye movement. If the damage occurs in the spinal cord, it can result in symptoms such as muscle weakness, numbness, or difficulty with coordination and balance. The unpredictable nature of these attacks, both in timing and location, is why MS symptoms can vary so widely among individuals and can change over time for a single person. The cumulative damage to myelin and the underlying nerve fibers can eventually lead to permanent neurological disability.

The autoimmune attack in MS is complex and involves several types of immune cells. The primary orchestrators are thought to be T-cells, a type of white blood cell. Specifically, helper T-cells become activated against myelin components and cross the blood-brain barrier. Once in the brain, they release inflammatory signals that recruit other immune cells. B-cells also play a critical role by producing antibodies that tag the myelin sheath for destruction and by presenting myelin antigens to T-cells, further fueling the inflammatory cascade. Additionally, microglia, the resident immune cells of the brain, become activated and contribute to the inflammation and tissue damage by engulfing myelin debris and releasing toxic molecules.

The exact cause of MS remains unknown, but it is widely accepted to be a multifactorial condition resulting from a combination of genetic and environmental factors. Genetically, certain variations in genes, particularly in the human leukocyte antigen (HLA) system which helps the immune system distinguish self from non-self, are associated with an increased risk. Environmentally, several triggers have been identified. Infection with the Epstein-Barr virus (EBV) is a significant risk factor. Low levels of vitamin D, which is important for immune regulation, are also strongly linked to an increased risk of developing MS. Furthermore, lifestyle factors such as cigarette smoking are known to increase both the risk of developing MS and its progression.

The central nervous system does have a natural capacity for repair through a process called remyelination. In this process, specialized stem cells in the brain, called oligodendrocyte precursor cells (OPCs), are activated. These cells migrate to the areas of demyelination, mature into new oligodendrocytes, and begin to produce new myelin sheaths to wrap around the exposed nerve fibers. In the early stages of relapsing-remitting MS, this repair mechanism can be quite effective, leading to the recovery of function and the periods of remission that patients experience. However, as the disease progresses, this remyelination process becomes less efficient. The chronic inflammation, depletion of OPCs, and formation of scar tissue create an environment that is hostile to repair. Consequently, the damage outpaces the body's ability to heal, leading to the accumulation of permanent nerve damage and the progressive worsening of symptoms. A major focus of current MS research is to find therapies that can protect nerves from damage and enhance the body's natural remyelination capabilities.