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Abstract
Multiple sclerosis (MS) develops in young adults with a complex predisposing genetic
trait and probably requires an inciting environmental insult such as a viral infection
to trigger the disease. The activation of CD4+ autoreactive T cells and their differentiation
into a Th1 phenotype are a crucial events in the initial steps, and these cells are
probably also important players in the long-term evolution of the disease. Damage
of the target tissue, the central nervous system, is, however, most likely mediated
by other components of the immune system, such as antibodies, complement, CD8+ T cells,
and factors produced by innate immune cells. Perturbations in immunomodulatory networks
that include Th2 cells, regulatory CD4+ T cells, NK cells, and others may in part
be responsible for the relapsing-remitting or chronic progressive nature of the disease.
However, an important paradigmatic shift in the study of MS has occurred in the past
decade. It is now clear that MS is not just a disease of the immune system, but that
factors contributed by the central nervous system are equally important and must be
considered in the future.
[1
]Cellular Immunology Section, Neuroimmunology Branch, National Institute of Neurological
Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892-1400;
email: ;