CD4 and Guillain-Barre syndrome: On the other hand, recent evidence that IFN-γ could convert peripheral CD4(+)CD25(−) T cells to CD4(+)CD25(+) regulatory T cells in GBS [41] and IFN-γ deficiency exacerbated EAN via upregulating Th17 cells despite a mitigated systemic Th1 immune response [42] defined an anti-inflammatory role for IFN-γ.