“…Although the pathogenic mechanism of GD-IRIS is not completely known, it seems to be a consequence of an immunoregulatory disequilibrium, characterized by thymic enlargement, failure of thymic deletion of autoreactive T-cells, persistence of T-cell receptor excision circle levels in CD4 and lymphocytes T CD8+ (CD8), and high circulating levels of naïve CD8 [ 59 , 65 ]. It seems that immune reconstitution promotes a profile shift in cytokines production from TH2 to TH1 types, permissive for the development of autoimmunity events [ 66 ].…”