IL-12 has been shown to diminish Treg suppressive capacity in inflammatory settings, shifting the balance toward effector responses.78 This pro-inflammatory shift was further reinforced by reduced expression of IL10 and its receptor IL10R, consistent with impaired regulatory B-cell function described in MS.79 EBV-positive cells also increased IL16, IL6ST (gp130), and IL6R, molecules implicated in MS pathogenesis, and upregulated the chemokine receptors CCR6 and CXCR3, which position B cells within Th17- and Th1-rich inflammatory niches rather than homeostatic environments. This evidence concerns the gene CCR6 and myeloid sarcoma.