Parasitic infections frequently result in highly polarized CD4(+) T cell responses characterized by dominant Th1 or Th2 cytokine production profiles. Although previously thought to be strictly dependent on signaling by the differentiative cytokines, IL-12 and IL-4, recent data indicate that this polarization may be primarily decided instead by a series of different factors intrinsic to the pathogen-antigen-presenting-cell interaction that influence T cell priming.