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Noureddin M, Zelber-Sagi S, Wilkens LR, Porcel J, Boushey CJ, Le Marchand L, et al

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In summary, through tryptophan degradation resulting from increased IDO and ROS activity in antigen-presenting cells, EBV-infected ectopic lymphoid aggregates can enhance differentiation into Th2 over Th1 and into Treg over Th17, thus creating an environment dominated by the release of anti-inflammatory cytokines (IL-10, IL-4, and TGF-) that decreases the antiviral adaptive response and favors immune tolerance and the development of autoimmune diseases [325], as it could lead to an increase in EBV-infected cells that could present autoantigens or viral EBNA-1 through MHC-II, which can undergo posttranslational modifications and form neoantigens that generate autoreactive responses [171, 212,213,214,215]

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A 2016 trial by Zubair et al