The immune system displays both enormous diversity and extraordinary specificity. It can recognize millions of distinctive foreign molecules and produce its own molecules and cells to match up with and counteract each of them. In order to have room for enough cells to match the millions of possible foreign invaders, the immune system stores just a few cells for each specific antigen.
When an antigen appears, those few specifically matched cells are stimulated to multiply into a full-scale army. Later, to prevent this army from overexpanding, powerful mechanisms to suppress the immune response come into play.
T cells, so named because they are processed in the thymus, appear to play a particularly important role in MS. They travel widely and continuously throughout the body patrolling for foreign invaders. In order to recognize and respond to each specific antigen, each T cell's surface carries special receptor molecules for particular antigens.
T cells contribute to the body's defenses in two major ways. Regulatory T cells help orchestrate the elaborate immune system. For instance, they assist other cells to make antibodies, proteins programmed to match one specific antigen much as a key matches a lock. Antibodies typically interact with circulating antigens, such as bacteria, but are unable to penetrate living cells. Chief among the regulatory T cells are those known as helper (or inducer) cells. Helper T cells are essential for activating the body's defenses against foreign substances. Yet another subset of regulatory T cells acts to turn off, or suppress, various immune system cells when their job is done.
Killer T cells, on the other hand, directly attack diseased or damaged body cells by binding to them and bombarding them with lethal chemicals called cytokines. Since T cells can attack cells directly, they must be able to discriminate between "self" cells (those of the body) and "nonself" cells (foreign invaders). To enable the immune system to distinguish the self, each body cell carries identifying molecules on its surface. T cells likely to react against the self are usually eliminated before leaving the thymus; the remaining T cells recognize the molecular markers and coexist peaceably with body tissues in a state of self-tolerance.
In autoimmune diseases such as MS, the detente between the immune system and the body is disrupted when the immune system seems to wrongly identify self as nonself and declares war on the part of the body (myelin) it no longer recognizes. Through intensive research efforts, scientists are unraveling the complex secrets of the malfunctioning immune system of patients with MS.
Components of myelin such as myelin basic protein have been the focus of much research because, when injected into laboratory animals, they can precipitate experimental allergic encephalomyelitis (EAE), a chronic relapsing brain and spinal cord disease that resembles MS. The injected myelin probably stimulates the immune system to produce anti-myelin T cells that attack the animal's own myelin.
Investigators are also looking for abnormalities or malfunctions in the blood/brain barrier, a protective membrane that controls the passage of substances from the blood into the central nervous system. It is possible that, in MS, components of the immune system get through the barrier and cause nervous system damage.
Scientists have studied a number of infectious agents (such as viruses) that have been suspected of causing MS, but have been unable to implicate any one particular agent. Viral infections are usually accompanied by inflammation and the production of gamma interferon, a naturally occurring body chemical that has been shown to worsen the clinical course of MS. It is possible that the immune response to viral infections may themselves precipitate an MS attack. There seems to be little doubt that something in the environment is involved in triggering MS.
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