Characterizing effector cells at the host:parasite interface

BALB/c mice develop chronic infection upon exposure to the intestinal helminth Heligmosomoides polygyrus ; the rapid clearance of subsequent re‐infection is a model for the Th2‐polarized memory response. Using immunofluorescence microscopy and laser microdissection‐assisted real‐time PCR, we examined the immune cell infiltrate surrounding the invading parasite at day 4 post‐infection, in order to identify potential effector cells mediating worm expulsion. Whereas infection in naïve mice resulted in a homogeneous Gr‐1 high infiltrate, the response to infection in previously immunized mice was characterized by three CD11b + populations with distinct patterns of Gr‐1 and F4/80 expression and located in specific regions surrounding the parasite. One of these populations stained positive for markers of alternatively activated macrophages (AAMΦ), and another population stained Gr‐1 + /F4/80 + , suggestive of inflammatory macrophages. Blockade of the Arginase‐1 pathway characteristic of AAMΦ resulted in abrogation of the protective memory response to H. polygyrus , as measured by worm and egg burdens 14 days post‐infection. Ongoing studies are examining the effects of selective depletion of specific Gr‐1 cell populations. These studies indicate the development of a distinct, localized, memory Th2 inflammatory response at the host:parasite interface shortly after infection, a subpopulation of which is required for worm expulsion.