IL-10 is elevated in the initial phase of TBE, but in severe course of disease, especially at later days of infection, IL-10 levels in the cerebrospinal fluid of TBEV-infected patients are reduced, which may contribute to a decrease in IFN-γ synthesis and act as an immunosuppression stimulant promoting inhibition of type 1 pro-inflammatory cytokine cascade. Here, IL10 is linked to tick-borne encephalitis.