Infection of mice lacking interleukin-7 (IL-7) reveals an unexpected role for IL-7 in the development of the parasite Schistosoma mansoni

A single intradermal administration of recombinant interleukin-7 (IL-7) has been shown to aggravate the course of murine schistosomiasis, to favor the development of Th2-associated antibodies specific for the parasite, and to alter migration kinetics and/or migratory route of the parasite within its vertebrate host. Here we show that after infection of IL-7-deficient mice with Schistosoma mansoni, the predominant parasite-specific humoral respons e follows a Th1 pattern, and the development of the parasite is greatly imp aired. In IL-7-deficient mice, increased numbers of larvae reach the lungs and fewer larvae reach the liver, compared to control mice. In the absence of IL-7, female worms show an altered fecundity, leading to decreased numbe rs of eggs trapped in the tissues and to an amelioration of the pathology o f the infected host. The most striking observation is the blockade of paras ite growth in an IL-7-defective environment, leading to dwarf male and fema le worms. The results of this study have important implications for the rol e of IL-7 in the host-parasite relationship and show how parasites can disa ble or evade the host immune response.