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. Author manuscript; available in PMC: 2015 Jun 15.
Published in final edited form as: Nat Rev Neurol. 2012 Oct 9;8(11):602–612. doi: 10.1038/nrneurol.2012.198

Figure 3.

Figure 3

Potential mechanisms by which Epstein-Barr virus infection might contribute to the development of multiple sclerosis. Patients with MS show higher frequencies and activation states of self-reactive lymphocytes (red nuclei), in addition to impaired functions of regulatory immune compartments indicating a lower threshold for breakdown of self-tolerance to central nervous system (CNS) antigens. Strong innate immune activation during primary EBV infection (virions and viral DNA are depicted as red dots) could facilitate the activation and expansion of autoreactive and polyspecific (i.e. both autoantigen and viral antigen specific) T and B cells. These cells could be maintained in the presence of continuous antigen exposure. In addition, latent EBV infection confers B cell survival advantages and could rescue autoreactive B cells from apoptotic deletion during B cell development and differentiation. Homing of these rescued autoreactive lymphocytes, which have immunomodulatory and antigen-presenting functions on T cells, to the inflamed CNS might contribute to the immunopathology of MS.