IFNG and experimental autoimmune encephalomyelitis: Despite promoting Th2 cytokine production, enhancing the regulatory function of Treg and suppressing the expression of the pro-inflammatory cytokines TNF-α, IL-12, and IFNγ under certain experimental conditions, IL-9 is also able to expand Th17 cell population and to promote inflammation, as the adoptive transfer of Th9-polarized cells induces experimental autoimmune encephalomyelitis and experimental autoimmune uveitis [38, 41].