Importance of interferon-γ in protective immunity against Hymenolepis nana cysticercoids derived from challenge infection with eggs in [formula omitted] mice

Abstract

The function of cytokines produced during Hymenolepis nana egg infection in mice in protective immunity against re-infection was examined. Treatment of mice with monoclonal antibody (MAb) against mouse interferon (IFN)-γ caused suppression of protective immunity against H. nana re-infection when the MAb was injected intraperitoneally at a daily dose of 40.0 mg kg −1 during the effector phase of protective immunity. Although high levels of IFN-γ, tumour necrosis factor (TNF)-α and interleukin (IL)-1β were released into the intestinal tracts of the parasitised mice at challenge infection, there was almost no release of these cytokines in mice treated with the MAb. Daily administration of rolipram failed to suppress the protective immunity, even when 400 μg kg −1 of the agent was administered into mice during the effector phase of immunity. Treatment of mice with rolipram completely suppressed both TNF-α and IL-1β production in intestinal tracts, induced by H. nana challenge infection. However, endogenous IFN-γ production in the intestine was scarcely affected by rolipram. These results strongly suggest that IFN-γ is the most important (or essential) cytokine in protective immunity to H. nana re-infection, rather than TNF-α and IL-1β.