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Hypothesis
January 2003

Are Astrocytes Central Players in the Pathophysiology of Multiple Sclerosis?

Author Affiliations

From the Departments of Neurology, Academisch Ziekenhuis Groningen, Groningen, the Netherlands (Drs De Keyser and Zeinstra), and University of Texas Southwestern Medical Center at Dallas (Dr Frohman).

Arch Neurol. 2003;60(1):132-136. doi:10.1001/archneur.60.1.132
Abstract

An interaction between antimyelin T cells and antigen-presenting glial cells is a crucial step in the cascade of immune events that lead to the inflammatory lesions in multiple sclerosis (MS). One of the most debated and controversial issues is whether microglial cells or astrocytes are the key players in initiating the (auto)immune reactions in the central nervous system in MS. Many investigators consider microglia to be the responsible intrinsic immunoeffector cells. In this review, we speculate that in MS astrocytes may serve as primary (facultative) antigen-presenting cells due to a failure of noradrenergic suppression of class II major histocompatibility complex molecules, which is caused by a loss of β2-adrenergic receptors. If this hypothesis is correct, pharmacologic suppression of the antigen-presenting capacities of astrocytes may be a potential therapy for MS.

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