“…Principally, upon experimental infection, immunocompetent mice elicit a cell-mediated immune response, which is so far inefficient as it impairs, but does not inhibit, the proliferation of the metacestode (Dai et al, 2004;Mejri et al, 2010). It has been shown that the type of the primary immune response toward infection, initially Th1-oriented, got progressively Th2-oriented (Mejri et al, 2011a) during the progressive growth of the metacestode, leading to the chronic stage of AE. Concomitantly, intraperitoneal dendritic cells (DCs) and T cells isolated at this late stage of infection expressed relatively high levels of TGF- mRNA, while IFN-␥ mRNA, and the surface expression of the major costimulatory molecules CD80, CD86, CD40 and the MHC class II (Ia) molecules were downregulated (Mejri et al, 2011a,b).…”