When we compared the cytokine/chemokine profile in different encephalitis groups, patients with ADEM showed predominant elevation of Th1 (IFN-γ, TNF-α, CXCL9, CXCL10), Th2 (IL-4, Eotaxin, CCL17, IL-13), Th17 (IL-23, G-CSF, IL-6, IL-8 and IL-17A), B cell (CXCL13, BAFF, CCL19) and other cytokines (CXCL1, IFN-α 2, IL-1ra) molecules, which supports the hypothesis that both cell mediated and humoral effector mechanisms may play a role in this condition, similar to experimental allergic encephalomyelitis (EAE) model in mouse [29, 30]. This evidence concerns the gene CCL19 and acute disseminated encephalomyelitis.