Multiple Sclerosis and the Immune System

Multiple Sclerosis and the Immune SystemMultiple Sclerosis (MS) is a debilitating, autoimmune disease which causes lesions and plaques throughout the nervous system. It is caused by self-reacting immune cells attacking neurons in the brain and spinal cord, as well as peripheral nerves, forming lesions or plaques at the site of damage.

Patients with multiple sclerosis develop a wide range of neurological and psychiatric symptoms. Loss of sensitivity, loss of vision, muscle spasms, ataxia, speech difficulties, and chronic pain are common deficits, many of which become irreversible as the disease progresses. Loss of muscle control follows damage to nerves and can lead to respiratory failure and death.

The thymic gland plays a critical role in preventing self-reactive immune cells from escaping programmed cell death. Through a process of thymic selection, the body presents endogenous protein components to developing immune cells, in order to impart self-peptide (protein) tolerance.

Within the medulla of the thymus, immature T-cells are presented endogenous protein component. Those that bind too strongly to these components during cortex-specific pathways of antigen processing are eliminated, otherwise, if released, they would target and damage organs, tissues and nerves. This is one of the most important roles of the thymus. However, in patients with multiple sclerosis, auto-reactive immune cells escape the thymus and target and damage myelin basic protein (MBP), a protein found in sheaths enclosing nerves.

Multiple Sclerosis is considered a relapsing and remitting disease, as it can be progressive or in remission. Between attacks, symptoms may decrease; however, permanent damage persists and accumulates over time. Life expectancy for MS is 5-10 years lower compared to the general population and no known cures are presently available; however, methods to increase rates of remission are currently under development.