This chapter from Multiple Scleroris for the Non-Neurologist approaches the subject of immunology of multiple sclerosis from the standpoint of available acute and disease modifying therapies and currently known immunologic targets for them.
This author proposes to approach the subject of immunology of multiple sclerosis (MS) from the standpoint of available acute and diseasemodifying therapies (DMTs) and currently known immunologic targets for them.
This seems to be a sound approach because historically this vision point has helped to shape and direct our knowledge on MS immunology and has developed and enriched the field over the years.
Another good reason to adopt this approach is its immediate applicability. By engaging this view, we learn not only MS immunology but also how various different medications work. And we not only learn how they work (in other words, mechanism of action or MoA of DMTs) but also come very close to understanding their potential efficacy, risks, and side effects. This strategic approach will serve well in understanding emerging MS therapies.
Unlike many other diseases of the immune system, such as lupus, psoriasis, or rheumatoid arthritis, MS has a single target, and that is myelin. Therefore, we do not expect to see multiple different tissues involved—the immune system and central nervous system (CNS) are the fields where the events take place.
Contrary to many patients’ beliefs, MS is not a disease of a “weak” immune system; it is a disease of a mistaken immune system. In fact, immune reactions in MS can prove to be very strong, leading to remarkable CNS inflammatory reactions and subsequent damage. But the initial “intentions” of the activated immune system are “good”; it intends to “protect” the human, the host. There is a hypothesis of strong initial inflammatory reaction, which leads to cascades of delayed events in the immune system; for example, one may have had an episode of acute infection, such as, for example, mononucleosis, which made a particularly strong and lasting impression on the immune system, and ever since that episode the immune system gets itself activated trying to find the offending agent, virus or bacteria, for weeks, months, or even years and decades after this particular infection is over. The overzealous protective efforts may get so intense that even mere resemblance to the offending antigen (e.g., the encounter of biochemical structures similar to the structures of relevant viral molecules) may be sufficient to trigger a very strong and destructive immune reaction. The most acute form of inflammation in MS clinically presents itself as a relapse or exacerbation.
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