Multiple studies have demonstrated the role of CXCR3 and its ligands in the migration of activated T cells during Th1 immune responses including to sites of infection [75, 76] . It is also known that the chemokines CXCL9 and CXCL10 are induced by the presence of the proinflammatory cytokine, IFN-c [34, 36, 37, 77] . More recently, however, the function of this family of chemokines has expanded to include neural-glial signaling following brain lesion where injured neurons upregulate CXCL10 and recruit CXCR3 expressing microglia to phagocytose denervated dendrites [33] . Consistent with this, another recent study has implicated CXCR3 in the function of perivascular macrophages and their ability to remodel the vasculature during stress [78] . We noted upregulation of CXCR3, CXCL9 and CXCL10 in the brain during chronic Toxoplasma infection. Furthermore, CXCR3 was preferentially expressed on macrophages expressing the scavenger receptors MMR and stabilin-1, suggesting an alternatively activated phenotype for these cells. Previous studies have established important functions of AAMØ in the context of helminth infection and wound healing [43, 79, 80] however not during an infection that generates such a polarized Th1 immune response such as Toxoplasma. T. gondii is known to exploit the arginine metabolic pathway and induce arginase-1 expression in macrophages thereby suppressing nitric oxide production but this does not lead to the alternative activation of these cells [46] [47] [48] . Instead our data point to a role for the cyst being the source of alternative activation of macrophages and the subsequent ability of these cells to lyse cysts via destruction of the chitin in the cyst wall. Thus, we observed a contact dependent significant increase in arginase activity following treatment with cysts and cystAg suggesting that this induction is not a result of infection by the replicating parasite, but rather by the presence of chitin in the cyst wall. The weak induction of arginase activity observed also points to a limited role for arginase-1 in the chitin-induced phenotype.