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Arch Neurol. 2006;63:810-811.

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

Although the cause of multiple sclerosis (MS) is unknown, clinical and pathologic evidence strongly suggest a link between an infectious agent and an autoimmune response directed against myelin.^1-3 Epidemiologic studies also have implicated an environmental factor, most likely an infectious agent, as a necessary element in the development of MS.² One possibility is that antigens from infectious pathogens may activate autoreactive T cells, causing them to expand and leading to clinical autoimmune disease.^4-5 However, molecular mimicry (as this process is termed) has found limited empirical support as a general mechanism to explain the origin and course of a broad range of autoimmune diseases. Another possibility is that rather than there being a specific pathogen causing MS, infections in and of themselves may be able to aggravate autoimmune processes. For example, infectious processes such as Chlamydia pneumoniae can activate antigen-presenting cells and consequently activate autoreactive T cells that do not cross-react . . . [Full Text of this Article]

AUTHOR INFORMATION

Amy E. Lovett-Racke, PhD; Michael K. Racke, MD

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