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Multiple sclerosis (MS) is the most common and disabling neurological disease of young adults. Currently more than 1.2 million people are affected worldwide, and the relapsing-remitting form of MS is three times more common in females than males. There are several lines of evidence to suggest that MS is an autoimmune disease which may be modified by genetic factors (see Compston et al1). However it has taken more than a century after the first systematic description of MS by English and French neurologists for any progress to be made in treatment.
The currently available immunomodulatory treatments, interferon-beta (IFN-β) and glatiramer acetate, are reasonably safe but unfortunately only partially effective.1 There is no doubt that better and more effective therapies are needed. The development of new agents has been aided by a better understanding of immunopathogenetic subtypes of MS,2,3 improvement in MS trial methodology and MRI techniques,4 and research on novel biomarkers.5
The complexity of MS precludes simplistic therapeutic approaches. Traditionally, immunologists have used the animal model of experimental autoimmune encephalomyelitis (EAE) for therapeutic studies, since it can reproduce many of the specific neuropathological and immunological aspects of MS. Despite its obvious limitations,6,7 including the fact that EAE is typically not spontaneous but induced by active sensitisation with brain tissue antigens, EAE is still a useful tool for developing new therapies. In particular, the model has helped to identify different phases and mechanisms of the autoimmune attack, which can be targeted with selective immunotherapeutic approaches. As a consequence, and within a short time, a growing number of “immunobiologicals” have been introduced into clinical MS studies.
VLA-4 AS A THERAPEUTIC TARGET IN MULTIPLE SCLEROSIS
Mode of action
In striking contrast to previous concepts, which viewed the central nervous system (CNS) as an “immunopriviledged” site completely occluded from the immune system, it is now …
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