An important feature of AAMØ is the cell's ability to produce arginase-1, which acts on its substrate, L-arginine to produce Lornithine, a precursor to collagen [43] . L-arginine is also the substrate for NO synthase and the two enzymes compete for substrate availability and are regulated by Th1 and Th2 type cytokines [44, 45] . Previous studies have demonstrated that direct infection of macrophages by T. gondii tachyzoites can induce arginase expression via STAT-6 dependent and independent pathways [46] [47] [48] . Furthermore these studies imply that such an induction is a survival strategy enlisted by the parasite to inhibit killing via NO. To assess whether or not macrophages and microglia in the infected brain produce arginase, CD11b+ BMNCs from infected mice were isolated and analyzed for arginase-1 expression by qRT-PCR. Our results show almost a 2fold increase in arginase-1 expression in cells from infected brains over naïve ( Figure 1K ). Thus, during chronic T. gondii infection there is a population of AAMØ in the CNS characterized by expression of CXCR3, MMR, stabilin-1 and the production of arginase-1.