CD8+ cells protect mice against reinfection with the intestinal parasite Eimeria falciformis

Pogonka, Thomas; Schelzke, Katja; Stange, Jörg; Papadakis, Konstantin; Steinfelder, Svenja; Liesenfeld, Oliver; Lucius, Richard

doi:10.1016/j.micinf.2009.12.005

Cited by 17 publications

(20 citation statements)

References 31 publications

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“…IL-22 has recently been shown to have anti-parasite effect in the gut as well (101). IFN-γ is required for the control of intracellular apicomplexan parasite Eimeria falciformis (102). In Ifngr -deficient mice, neutralization of IL-22 alone can increase the parasite burden, suggesting an important anti-parasitic role of IL-22.…”

Section: Effector Functions Of Rorγt+ Ilcs In the Gutmentioning

confidence: 99%

Aryl hydrocarbon receptor promotes RORγt+ Group 3 ILCs and controls intestinal immunity and inflammation

Qiu

Zhou

2013

Semin Immunopathol

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Unlike adaptive immune cells that require antigen recognition and functional maturation during infection, innate lymphoid cells (ILCs) usually respond to pathogens promptly and serve as the first line of defense in infectious diseases. RAR-related orphan receptors (RORγt)+ ILCs are one of the innate cell populations that have recently been intensively studied. During the fetal stage of development, RORγt+ ILCs (e.g., lymphoid tissue inducer-LTi cells) are required for lymphoid organogenesis. In adult mice, RORγt+ ILCs are abundantly present in the gut to exert immune defensive functions. Under certain circumstances, however, RORγt+ ILCs can be pathogenic and contribute to intestinal inflammation. Aryl hydrocarbon receptor (Ahr), a ligand-dependent transcriptional factor, is widely expressed by various immune and non-immune cells. In the gut, the ligand for Ahr can be derived/generated from diet, microflora, and/or host cells. Ahr has been shown to regulate different cell populations in the immune system including RORγt+ ILCs, T helper (Th)17/22 cells, γδT cells, regulatory T cells (Tregs), Tr1 cells, and antigen presenting cells (APCs). In this review, we will focus on the development and function of RORγt+ ILCs, and discuss the role of Ahr in intestinal immunity and inflammation in mice and in humans. Better understanding the function of Ahr in the gut is important for developing new therapeutic means to target Ahr in future treatment of infectious and autoimmune diseases.

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Section: Effector Functions Of Rorγt+ Ilcs In the Gutmentioning

confidence: 99%

Aryl hydrocarbon receptor promotes RORγt+ Group 3 ILCs and controls intestinal immunity and inflammation

Qiu

Zhou

2013

Semin Immunopathol

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“…All experiments were performed in accordance with the National Animal Protection Guidelines, approved by the Animal Ethics Committee. E. falciformis was maintained by serial passage in NMRI mice, bred at the Department of Molecular Parasitology (Humboldt University of Berlin), and oocysts were purified by flotation in sodium hypochloride as described elsewhere (2).…”

Section: Mice and Parasitesmentioning

confidence: 99%

“…(1)(2)(3)(4). IFN-g is a potent proinflammatory cytokine derived from multiple cells of both the innate and adaptive immune system, including CD4 + Th1 cells, CD8 + T cells, and NK cells.…”

mentioning

confidence: 99%

“…are of economic relevance, particularly in the poultry industry, with the costs attributed to lost revenue and drug treatment estimated to be in excess of £2 billion per year worldwide (19). Administration of infective oocysts via the natural oral route typically leads to the rapid development of an IFN-g-dominated response, which is associated with body weight loss and the development of transient inflammation and immunopathology in the large intestine (2). Although adoptive transfer of IFN-g-producing CD8…”

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confidence: 99%

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IL-22 Mediates Host Defense against an Intestinal Intracellular Parasite in the Absence of IFN-γ at the Cost of Th17-Driven Immunopathology

Stange

Hepworth

Rausch

et al. 2012

The Journal of Immunology

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The roles of Th1 and Th17 responses as mediators of host protection and pathology in the intestine are the subjects of intense research. In this study, we investigated a model of intestinal inflammation driven by the intracellular apicomplexan parasite Eimeria falciformis. Although IFN-γ was the predominant cytokine during E. falciformis infection in wild-type mice, it was found to be dispensable for host defense and the development of intestinal inflammation. E. falciformis-infected IFN-γR−/− and IFN-γ−/− mice developed dramatically exacerbated body weight loss and intestinal pathology, but they surprisingly harbored fewer parasites. This was associated with a striking increase in parasite-specific IL-17A and IL-22 production in the mesenteric lymph nodes and intestine. CD4+ T cells were found to be the source of IL-17A and IL-22, which drove the recruitment of neutrophils and increased tissue expression of anti-microbial peptides (RegIIIβ, RegIIIγ) and matrix metalloproteinase 9. Concurrent neutralization of IL-17A and IL-22 in E. falciformis-infected IFN-γR−/− mice resulted in a reduction in infection-induced body weight loss and inflammation and significantly increased parasite shedding. In contrast, neutralization of IL-22 alone was sufficient to increase parasite burden, but it had no effect on body weight loss. Treatment of an E. falciformis-infected intestinal epithelial cell line with IFN-γ, IL-17A, or IL-22 significantly reduced parasite development in vitro. Taken together, to our knowledge these data demonstrate for the first time an antiparasite effect of IL-22 during an intestinal infection, and they suggest that IL-17A and IL-22 have redundant roles in driving intestinal pathology in the absence of IFN-γ signaling.

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“…Detailed mechanisms of the innate immunity against Eimeria infection are still unknown. However, IFN-γ and NK cells known as a source of IFN-γ have been indicated to play a protective role in innate and adaptive immunity to Eimeria and Cryptosporidium infections (Barakat et al 2009, Pogonka et al 2010, Rose et al 1989, Rose et al 1984, Schito and Barta 1997, Smith and Hayday 2000. In the experiment using beige mice, it was shown by the obvious increase in their mortality rate that the NK cell is important in resistance to a primary infection of E. krijgsmanni.…”

Section: Resultsmentioning

confidence: 99%

Host specificity and in vivo infectivities of the mouse coccidian parasites Eimeria krijgsmanni

Hashimoto

Tanaka

Matsubayashi

et al. 2014

Acta Parasitologica

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In the present study, infection experiments of E. krijgsmanni using various hosts were conducted to elucidate the host specificity among some animals and the infectivity to mouse strains. According to the results, the infection was not found in most animals, except for rats, in which some oocyst shedding was detected, and there was no significant difference in infectivity among mouse strains. Additionally, oocyst shedding was hardly detectable in a secondary infection to immunocompetent mice, although it was found in immunodeficient mice. These results indicated that only immunocompetent mice could develop adaptive immunity against reinfection by stimuli of the primary infection. Furthermore, the infection experiments were performed with splenic macrophage (Mφ)-depleted mice with a reagent and Beige (Bg) mice known to be a strain of mice with low NK cell activity. No significant effect was found in primary or secondary infections in the Mφ-depleted mice, whereas the mortality rate was clearly increased in Bg mice inoculated with a large number of oocysts. Their oocyst shedding was similar to that of immunocompetent hosts. Taken together, these results suggested that Mφ has only a minor role in the immune response, but the NK cell has an important function in resistance to primary infection of E. krijgsmanni.

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CD8+ cells protect mice against reinfection with the intestinal parasite Eimeria falciformis

Cited by 17 publications

References 31 publications

Aryl hydrocarbon receptor promotes RORγt+ Group 3 ILCs and controls intestinal immunity and inflammation

Aryl hydrocarbon receptor promotes RORγt+ Group 3 ILCs and controls intestinal immunity and inflammation

IL-22 Mediates Host Defense against an Intestinal Intracellular Parasite in the Absence of IFN-γ at the Cost of Th17-Driven Immunopathology

Host specificity and in vivo infectivities of the mouse coccidian parasites Eimeria krijgsmanni

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