Chitin is found in the exoskeletons of insects, fungal cell walls, sheaths of parasitic nematodes, and is a component of the T. gondii cyst wall [49, 50] . The presence of this exogenous molecule can induce the recruitment of AAMØ, basophils, neutrophils, and eosinophils [52, [81] [82] [83] [84] . Active chitinases such as AMCase and chitotriosidase are secreted by macrophages in response to chitincontaining pathogens and has been shown to inhibit hyphal growth of chitinous fungi such as Candida and Aspergillus [56, 58] . Despite the link between chitin and the recruitment of type 2 inflammation in the lung [52] , a recent study has demonstrated no role for AMCase in the generation of allergic airway pathology [85] . In this study we demonstrate for the first time, macrophage chitinase activity in response to a protozoan pathogen. Chitin recognition is thought to be a size dependent process and involve a combination of TLR2 and scavenger receptors such as MMR and dectin-1 [49, 58] . Here we have demonstrated the presence of such scavenger receptors in association with cysts and it will be of interest in future studies to determine the role of these molecules in cyst containment during Toxoplasma infection. Independent of the receptors involved it is likely that this is a contact-dependent process and indeed, cysts were unable to induce urea production or chitinase activity in macrophages when separated by transwell membranes. Furthermore, analysis of the location of AMCase producing cells in the brain finds them reliably close to cysts and often in direct contact with reactivating or rupturing cysts. These images show that despite the presence of many DAPI positive cells surrounding the cyst structure, the escape of parasites through the cyst wall occurs juxtaposed to the macrophage or AMCase activity. Our data suggest that the presence of cyst antigens induces alternative activation of macrophages and that these antigens are required for macrophages to produce chitinase even in the presence of IL-4. Thus alternative activation of macrophages is not sufficient for AMCase production and chitinase activity. The significant increase of the non-enzymatically active chitinase-like molecule YM-1 in infected brains is consistent with previous reports of AMCase and YM-1 being co-expressed specifically in macrophages and not epithelial cells [63] .