FASLG and experimental autoimmune encephalomyelitis: Consistent with previous observation that γδ T cells could express FasL at sites of inflammation and thus induce apoptosis of target cells [36], Ponomarev et al. found that, in the experimental autoimmune encephalomyelitis (EAE) model of the human CNS autoimmune disease multiple sclerosis, γδ T cells were able to regulate CNS inflammation and promote disease recovery through Fas/FasL-induced apoptosis of encephalitogenic T cells [19].