To further decipher the role of IL-17A on worm development in early phase of infection, we employed the rodent model of filariasis in C57BL/6 mice and demonstrate that infected IL-17A-deficient C57BL/6 mice develop longer but reduced numbers of adult worms and cell cultures secrete increased levels of filarial-specific IFN-γ. Here, IL17A is linked to filariasis.