No abstract

B cells can mediate protective responses against nematode parasites by supporting Th2 cell development and/or by producing Abs. To examine this, B cell-deficient mice were inoculated with Nippostrongylus brasiliensis or Heligmosomoides polygyrus. B cell-deficient and wild type mice showed similar elevations in Th2 cytokines and worm expulsion after N. brasiliensis inoculation. Worm expulsion was inhibited in H. polygyrus-inoculated B cell-deficient mice, although Th2 cytokine elevations in mucosal tissues were unaffected. Impaired larval migration and development was compromised as early as day 4 after H. polygyrus challenge, and administration of immune serum restored protective immunity in B cell-deficient mice, indicating a primary role for Ab. Immune serum even mediated protective effects when administered to naive mice prior to inoculation. This study suggests variability in the importance of B cells in mediating protection against intestinal nematode parasites, and it indicates an important role for Ab in resistance to tissue-dwelling parasites.

The protective immune response that develops following infection with many tissue-dwelling intestinal nematode parasites is characterized by elevations in IL-4 and IL-13 and increased numbers of CD4+ T cells, granulocytes and macrophages. These cells accumulate at the site of infection and in many cases can mediate resistance to these large multicellular pathogens. Recent studies suggest novel potential mechanisms mediated by these immune cell populations through their differential activation and ability to stimulate production of novel effector molecules. These newly discovered protective mechanisms may provide novel strategies to develop immunotherapies and vaccines against this group of pathogens. In this review, we will examine recent studies elucidating mechanisms of host protection against three widely-used experimental murine models of tissuedwelling intestinal nematode parasites: Heligmosomoides polygyrus, Trichuris muris and Trichinella spiralis.

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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‐1high 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.