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This abstract is assigned to session Academic session
TitleInfection and Autoimmune Disease in the CNS
PurposeImmune responses to challenge by foreign antigens depend not only on the nature of the challenge and the type of immune response, but are fashioned to a degree by the tissue in which they are initiated. This is especially so in the CNS which is considered "privileged" in the sense that foreign antigens, particularly alloantigens, may not be rejected or cleared as readily as they would be in non-privileged tissues such as the skin and lung. Pathogens which gain access to the CNS and its border tissues may benefit from its privileged status and persist as latent infections. Immune privilege (IP) is an active state dependent not only on specific barrier functions but on active immunoregulatory processes. When these fail, latent infections can reactivate with devastating consequences. Toxoplasmosis and CMV infections are clear examples of how the eye and the brain can be damaged when latent infections reactivate. More contentious is the role of latent infection in presumed autoimmune disease but the clinical presentation may provide clues. For instance, in cases of multiple sclerosis the pattern of disease correlates well with reactivation of latent Epstein Barr virus in CNS meningeal resident B cells. Moreover, the beneficial effects of B cell depletion in MS supports a pathogenic role for latently-infected B cells. A model implicating latent infection may therefore be a paradigm for the pathogenesis of autoimmune diseases generally.
Conflict of interestNo
Authors 1
CityAberdeen, Scotland, UK - Crawley, Western Australia
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