Figure 2

Models proposing the role of CCL21 during inflammation in the brain. (a) CCL19 and CCL21 expression at the blood–brain barrier (BBB) may aid extravasation of CCR7+ leukocytes. During pathogenic insults, CNS-resident glial cells induce CCL21 which in turn facilitates T-cell migration from the perivascular area to the site of infection to keep pathogens under control; (b) Ischemia- or glutamate-mediated damage causes neurons to release CCL21 from the primary lesion site to activate microglia through the CXCR3 receptor. CXCR3-CCL21 signaling-mediated neuroglial communication is a potent mechanism to activate glial cells that are present at a distant site from the lesion.