G-CSF treatment promotes apoptosis of autoreactive T cells to restrict the inflammatory cascade and accelerate recovery in experimental allergic encephalomyelitis
G-CSF inhibits inflammatory infiltration and demyelination in CNS of EAE mice. G-CSF prevents pro-inflammatory cytokine and NO productions, and increases IL-4 and IL-10 secretions. G-CSF suppresses autoreactive T cell proliferation through apoptosis. G-CSF induces resting G0/G1-phase into S-phase of autoreactive T cells to promote anti-inflammatory action. G-CSF elevates a CD4+ CD25+ T cell subset that displays potent neuroprotective effects.