Recent studies have identified a substantial increase in tissue remodeling in the brain during chronic T. gondii infection [8] . Additionally, there is a continuous need for the clearance of debris from ruptured cysts and dead cells in the brain [31] . To investigate if AAMØ, known for their role in tissue remodeling and homeostatic clearance, are present during such an event in the CNS, macrophage populations from the infected brain were phenotypically analyzed for the expression of known markers of alternative activation. One of the key molecules that has been associated with a tissue remodeling macrophage phenotype in the CNS is the expression of CXCR3 on microglia [32, 33] . CXCR3 is required for protective immune responses to T. gondii primarily due to its role in Th1 cell recruitment and most recently for T cell search strategies in the brain [34] [35] [36] [37] . Indeed CXCR3 and its ligands are significantly upregulated in the brain at a timepoint associated with significant T cell influx into the CNS following infection ( Figure S1A , B) with ,35% of T cells expressing CXCR3 ( Figure 1A ). However, in addition to this well characterized role on T cells, there is a small but distinct population of macrophages that express high levels of CXCR3 (,10% of total macrophages)( Figure 1B ). There is also constitutive, although lower, expression of CXCR3 by CNS resident microglia, which remains unchanged following infection ( Figure S1C ).