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Interleukin17A (IL-17A) is known to be involved in the host defense against pathogens and the pathogenesis of autoimmune diseases. Previously, we showed that excessive amounts of interferon gamma (IFN-γ) play an important role in the pathogenesis of the lethal effects ofToxoplasma gondii by inducing anaphylactic responses. In the study described in this report, we examined the effects of IL-17A deficiency on murine host defense against oralT. gondii infection. IL-17A-deficient C57BL/6 (B6) mice exhibited higher rates of mortality than wild-type (WT) mice during the acute phase ofT. gondii infection. CD4+ T cells in the mesenteric lymph nodes (mLNs) and ileum ofT. gondii -infected IL-17A-deficient mice produced higher levels of IFN-γ than did those of WT mice. In addition, the level ofT. gondii HSP70 (T.g .HSP70) expression was also significantly increased in the ileum, mLNs, liver, and spleen of infected IL-17A-deficient mice compared with that in WT mice. These elevated levels of expression ofT.g .HSP70 and IFN-γ in infected IL-17A-deficient mice were presumably linked to the IL-17A defect since they decreased to WT levels after treatment with recombinant IL-17A. Furthermore, IL-17A-deficient mice were highly susceptible to the anaphylactic effect ofT.g .HSP70, and the survival of IL-17A-deficient mice during the acute phase was improved by treatment with an anti-T.g .HSP70 monoclonal antibody. These results suggest that IL-17A plays an important role in host survival againstT. gondii infection by protecting the host from an anaphylactic reaction via the downregulation ofT.g .HSP70 and IFN-γ production.

infection and immunity

Interleukin-17A-Deficient Mice Are Highly Susceptible to Toxoplasma gondii Infection Due to Excessively Induced T. gondii HSP70 and Interferon Gamma Production