In the JE model, the severity of encephalitis is related to skewing of the specific cellular response from regulatory (Treg) to Th17-type, with the increased IL-17, CXCL1, and CXCL2 expression promoting the CNS infiltration by granulocytes, monocytes, and cytotoxic CD8+ lymphocytes [50]. This evidence concerns the gene IL17A and viral encephalitis.