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. Author manuscript; available in PMC: 2013 Jun 27.
Published in final edited form as: Discov Med. 2011 Sep;12(64):213–228.

Figure 1.

Figure 1

Model for the role of T cells and astrocytes in the pathology of MS. Recent data suggest a necessary role for Th17 cells and astrocytes in EAE pathology. Activated myelin-specific Th17 cells of the central memory phenotype infiltrate the CNS and are restimulated to produce IL-17 by local dendritic cells to undergo clonal expansion and differentiation into effectors/effector memory T cells. Astrocytes respond via expression of IL-17R to T cell-released IL-17 and produce leukocyte-attracting chemokines in an Act1-dependent manner. Astrocyte-derived chemokines then recruit a second wave of peripheral inflammatory cells, which mediate EAE relapses and progression via Th17 cell-mediated bystander demyelination (adapted from Rodgers et al., 2010).