The pro-neutrophilic Th17 cytokines and chemokines signaling through CXCR1 and CXCR2 are upregulated intrathecally, and at least some of them (IL-17A) also systemically, starting from the peripheral and continuing into the neurologic phase of TBE, which allows them to exert their influence during the critical events deciding about the onset and severity of the CNS involvement. Here, CXCR2 is linked to tick-borne encephalitis.