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Infect Immun. 2017 Nov 17;85(12). pii: e00399-17. doi: 10.1128/IAI.00399-17. Print 2017 Dec.

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

Author information

1
Department of Infection and Host Defense, Graduate School of Medicine, Chiba University, Chiba, Japan.
2
Department of Infection and Host Defense, Graduate School of Medicine, Shinshu University, Matsumoto, Japan.
3
Center for Animal Disease Models, Research Institute for Biomedical Sciences, Tokyo University of Science, Noda, Japan.
4
Department of Molecular Pathology, Graduate School of Medicine, Shinshu University, Matsumoto, Japan.
5
Department of Infection and Host Defense, Graduate School of Medicine, Chiba University, Chiba, Japan faosai@shinshu-u.ac.jp.

Abstract

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 of Toxoplasma 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 oral T. gondii infection. IL-17A-deficient C57BL/6 (B6) mice exhibited higher rates of mortality than wild-type (WT) mice during the acute phase of T. gondii infection. CD4+ T cells in the mesenteric lymph nodes (mLNs) and ileum of T. gondii-infected IL-17A-deficient mice produced higher levels of IFN-γ than did those of WT mice. In addition, the level of T. gondii HSP70 (T.gHSP70) 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 of T.gHSP70 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 of T.gHSP70, and the survival of IL-17A-deficient mice during the acute phase was improved by treatment with an anti-T.gHSP70 monoclonal antibody. These results suggest that IL-17A plays an important role in host survival against T. gondii infection by protecting the host from an anaphylactic reaction via the downregulation of T.gHSP70 and IFN-γ production.

KEYWORDS:

IL-17; T. gondii HSP70; Toxoplasma gondii

PMID:
28893913
PMCID:
PMC5695131
DOI:
10.1128/IAI.00399-17
[Indexed for MEDLINE]
Free PMC Article

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