Ma et al. demonstrated that the suppressor of cytokine signaling 3 (Socs3) participates in IL17 functions in the CNS as a negative feedback regulator, using mouse models of Socs3 small interfering RNA (siRNA) knockdown and Socs3 deletion. These mice with loss of Socs3 function showed enhanced IL17 and IL6 signaling in astrocytes via the activation of the NF-κB and Mapk pathways, indicating that astrocytes can act as a target of Th17 cells and IL17 in the CNS [75] . Similarly, Kang et al. constructed specific deletion mutants of Act1, a critical component required for IL17 signaling, in mice with EAE to examine CNS inflammation in endothelial cells, macrophages, microglia, and the neuroectoderm (neurons, astrocytes, and oligodendrocytes). In these Act1-deficient mice, Th17 cells showed normal infiltration into the CNS but failed to recruit lymphocytes, neutrophils, and macrophages. Therefore, astrocytes are critical in IL17-Act1-mediated leukocyte recruitment during EAE [76] .