title: During acute experimental infection with the reticulotropic Trypanosoma cruzi strain Tulahuen IL-22 is induced IL-23-dependently but is dispensable for protection.
abstract: Protective immunity against Trypanosoma cruzi, the causative agent of Chagas disease, depends on the activation of macrophages by IFN-γ and IL-17A. In contrast, IL-10 prevents immunopathology. IL-22 belongs to the IL-10 cytokine family and has pleiotropic effects during host defense and immunopathology, however its role in protection and pathology during T. cruzi infection has not been analyzed yet. Therefore, we examined the role of IL-22 in experimental Chagas disease using the reticulotropic Tulahuen strain of T. cruzi. During infection, IL-22 is secreted by CD4-positive cells in an IL-23-dependent fashion. Infected IL-22(-/-) mice exhibited an increased production of IFN-γ and TNF and displayed enhanced numbers of activated IFN-γ-producing T cells in their spleens. Additionally, the production of IL-10 was increased in IL-22(-/-) mice upon infection. Macrophage activation and by association the parasitemia was not affected in the absence of IL-22. Apart from a transient increase in the body weight loss, infected IL-22(-/-) mice did not show any signs for an altered immunopathology during the first fourteen days of infection. Taken together, although IL-22 is expressed, it seems to play a minor role in protection and pathology during the acute systemic infection with the reticulotropic Tulahuen strain of T. cruzi.
authors.affiliation: Division of Infection Immunology, Research Centre Borstel, Borstel, Germany.|Priority Area Infection, Research Centre Borstel, Borstel, Germany.|Cluster of Excellence Inflammation-at-Interfaces (Borstel-Kiel-Lübeck-Plön), Germany.
authors.forename: Hanna
authors.initials: H
authors.lastname: Erdmann
authors.affiliation: Fluorescence Cytometry Core Facility, Research Centre Borstel, Borstel, Germany.
authors.forename: Jochen
authors.initials: J
authors.lastname: Behrends
authors.affiliation: Division of Infection Immunology, Research Centre Borstel, Borstel, Germany.|Priority Area Infection, Research Centre Borstel, Borstel, Germany.|Cluster of Excellence Inflammation-at-Interfaces (Borstel-Kiel-Lübeck-Plön), Germany.
authors.forename: Christoph
authors.initials: C
authors.lastname: Hölscher
mesh_terms: D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D014355:Chagas Disease / Q000276:immunology*; D016207:Cytokines / Q000276:immunology; D005260:Female; D007249:Inflammation; D016753:Interleukin-10 / Q000276:immunology; D053760:Interleukin-23 Subunit p19 / Q000276:immunology*; D007378:Interleukins / Q000276:immunology*; D007963:Leukocytes, Mononuclear / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D009154:Mutation; D018512:Parasitemia; D014349:Trypanosoma cruzi; D000097043:Interleukin-22
chemical_list: D016207:Cytokines; D016753:Interleukin-10; D053760:Interleukin-23 Subunit p19; D007378:Interleukins; D000097043:Interleukin-22; C556062:IL10 protein, mouse; C508841:Il23a protein, mouse