The observed pathways indicated that ERK activation triggered by CXCR3 signaling dampened the activation of NF-κB, a pivotal transcription factor crucial for the induction of IL-23 and CCL20, both necessary for Th17 cell expansion and recruitment and experimental autoimmune encephalomyelitis neuroinflammatory model (388). Here, CXCR3 is linked to experimental autoimmune encephalomyelitis.