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On Natalizumab, Dendritic Cells, and Dangerous Immune Privilege

Burkhard Becher, PhD

Arch Neurol. 2008;65(12):1566-1567.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Multiple sclerosis (MS) is the most common inflammatory disorder of the central nervous system (CNS), leading to progressive neurological deficit.¹ While most diseases of the CNS display some degree of inflammation involving CNS-resident innate immune cells (ie, microglia), MS is characterized by the invasion of adaptive immune cells (ie, lymphocytes) into the CNS parenchyma. It is now widely held that MS is an autoimmune disease in which encephalitogenic myelin-reactive T lymphocytes invade the neuropil and initiate an inflammatory cascade leading to demyelination and axonal loss. Current therapies for MS include immunomodulatory drugs such as glatiramer acetate or interferon β, and while some degree of alleviation can be achieved this way, we are still far away from a satisfactory therapeutic effect.² Rather than nonspecifically modulating immunity, an ideal therapeutic strategy would be to specifically inhibit autoimmunity while preserving the immune system's protective function against microbes and environmental hazards. . . . [Full Text of this Article]

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