Through this complex system of physical barriers, innate immunity, and adaptive immunity, the human organism is protected from most pathogens.
Unfortunately, sometimes the immune system fails to work as intended. One example of this is autoimmune disease. As stated earlier, an important characteristic of the immune system is the ability to distinguish self from non-self. It is normal to have some autoreactivity of the immune system. However, a normally functioning immune system will automatically delete autoreactive cells. Sometimes, and for reasons that are not clear, the normal regulatory mechanisms of the immune system become faulty. When the immune system cannot distinguish self from non-self, the stage is set for an auto or “selfreactive” immune disease.
Autoimmune diseases are numerous and heterogeneous. Although far from an exhaustive list, diseases such as psoriasis, Crohns disease, lupus erythematosis, myasthenia gravis and multiple sclerosis are considered autoimmune. Multiple sclerosis is often referred to as an immune-mediated disease, as a specific antigen that provokes the disease is not known.
The etiology of MS is not known, although it is thought to be a combination of a genetic susceptibility and an environmental exposure. This suggests some type of exposure, possibly to a virus in the environment that triggers the autoimmune behavior in a genetically susceptible individual.
Yet a specific virus and specific genes have not been completely identified. In MS, the target of the immune system becomes specific proteins located in the central nervous system. The targets are the myelin coating around axons, the axons themselves, and possibly the oligodendrocytes that make myelin. The immune system may confuse these self tissues with a similar-looking viral particle. Without the regulatory mechanisims to stop autoimmune activity, the immune system can become activated and target the central nervous system.
Activated immune system cells can become attracted to the target (the CNS) and through adhesion and disruption of the blood-brain barrier with various enzymes and cytokines, gain entry to the CNS. Activated T-cells, specifically Th-1 cells are then thought to orchestrate the immune response by recruiting and activating other immune system cells to the CNS. Inflammation is caused within the CNS, and this inflammatory response is damaging to myelin. Through direct damage and loss of the trophic support that myelin provides, underlying axons can also become damaged or destroyed.