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 with chlamydial antigens.6 The diversity of infectious agents associated with onset or exacerbation of clinical MS, the difficulty in identifying pathogen-associated antigens that activate autoreactive T cells, and the demonstration that antigen-presenting cell activation by infection can trigger an autoimmune response all suggest that the role of infection in autoimmunity may not be specific to a particular pathogen.
Lovett-Racke AE, Racke MK. Epstein-Barr Virus and Multiple Sclerosis. Arch Neurol. 2006;63(6):810–811. doi:https://doi.org/10.1001/archneur.63.6.810
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