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JEM

Once animals have experienced a helminthic infection, they often show stronger protective  immunity against subsequent infections. Although helminthic infections are well known to  elicit Th2-type immune responses, it remains ill-defined where and how acquired protection  is executed. Here we show that skin-invading larvae of the intestinal helminth Nippostrongylus brasiliensis are surrounded by skin-infiltrating cells and are prevented from migrating  out of infected skin during the second but not the first infection. B cell– or IgE receptor  FcRI–deficient mice showed impaired larval trapping in the skin. Selective ablation of  basophils, but not mast cells, abolished the larval trapping, leading to increased worm  burden in the lung and hence severe lung injury. Skin-infiltrating basophils produced IL-4  that in turn promoted the generation of M2-type macrophages, leading to the larval  trapping in the skin through arginase-1 production. Basophils had no apparent contribution  to worm expulsion from the intestine. This study thus reveals a novel mode of acquired  antihelminth immunity, in which IgE-armed basophils mediate skin trapping of larvae,  thereby limiting lung injury caused by larval migration.