In conclusion, the initial phase of TBE is associated with transitory laboratory abnormalities suggesting bone marrow as well as liver involvement and with rather heterogeneous response involving innate (CXCL11), B cell (CXCL13, BAFF), and T cell mediators (IL-27 and IL-4), whereas the second phase of TBE is characterized with angiogenic immune responses in serum and marked innate and Th1 adaptive immune responses in CSF implying that distinct processes play a role in the pathophysiology of different phases of TBE. This evidence concerns the gene CXCL11 and tick-borne encephalitis.