Differential <scp>IFN</scp>‐γ production by adult and neonatal blood <scp>CD</scp>56<sup>+</sup> natural killer (<scp>NK</scp>) and <scp>NK</scp>‐like‐<scp>T</scp> cells in response to <i><scp>T</scp>rypanosoma cruzi</i> and <scp>IL</scp>‐15

Guilmot, Aline; Carlier, Yves; Truyens, Carine

doi:10.1111/pim.12077

Cited by 13 publications

(8 citation statements)

References 32 publications

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“…Twarting such limitation requires an activation of fetal/neonatal monocytes and DCs. Monocytes produce IL-12 that synergizes with IL-15 to activate in turn NK cells and particularly the CD56 bright NK cell subpopulation releasing IFN-␥ (Guilmot et al, 2013(Guilmot et al, , 2014. DCs trigger T cell proliferation (preferentially CD8+ T cells) and more IFN-␥ release (Rodriguez et al, 2012a,b).…”

Section: Immune Responses In Congenitally Infected and Uninfected Newmentioning

confidence: 97%

Congenital Chagas disease as an ecological model of interactions between Trypanosoma cruzi parasites, pregnant women, placenta and fetuses

2015

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The aim of this paper is to discuss the main ecological interactions between the parasite Trypanosoma cruzi and its hosts, the mother and the fetus, leading to the transmission and development of congenital Chagas disease. One or several infecting strains of T. cruzi (with specific features) interact with: (i) the immune system of a pregnant woman whom responses depend on genetic and environmental factors, (ii) the placenta harboring its own defenses, and, finally, (iii) the fetal immune system displaying responses also susceptible to be modulated by maternal and environmental factors, as well as his own genetic background which is different from her mother. The severity of congenital Chagas disease depends on the magnitude of such final responses. The paper is mainly based on human data, but integrates also complementary observations obtained in experimental infections. It also focuses on important gaps in our knowledge of this congenital infection, such as the role of parasite diversity vs host genetic factors, as well as that of the maternal and placental microbiomes and the microbiome acquisition by infant in the control of infection. Investigations on these topics are needed in order to improve the programs aiming to diagnose, manage and control congenital Chagas disease.

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Section: Immune Responses In Congenitally Infected and Uninfected Newmentioning

confidence: 97%

Congenital Chagas disease as an ecological model of interactions between Trypanosoma cruzi parasites, pregnant women, placenta and fetuses

2015

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“…A greater frequency of mature NK cells was also observed in asymptomatic patients, as compared to cardiac patients, suggesting a contribution of this cell subset to the establishment and/or maintenance of the lack of symptoms during chronic infection ( 46 ). Additionally, peripheral and cord blood experimental infection assays highlighted NK cells as the most potent IFN-γ producing subset, besides also secreting IL-15 ( 69 ) in response to the pathogen, suggesting their relevance in the primary response to infection.…”

Section: Innate Immunitymentioning

confidence: 99%

The Unsolved Jigsaw Puzzle of the Immune Response in Chagas Disease

2018

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Trypanosoma cruzi interacts with the different arms of the innate and adaptive host's immune response in a very complex and flowery manner. The history of host-parasite co-evolution has provided this protozoan with means of resisting, escaping or subverting the mechanisms of immunity and establishing a chronic infection. Despite many decades of research on the subject, the infection remains incurable, and the factors that steer chronic Chagas disease from an asymptomatic state to clinical onset are still unclear. As the relationship between T. cruzi and the host immune system is intricate, so is the amount and diversity of scientific knowledge on the matter. Many of the mechanisms of immunity are fairly well understood, but unveiling the factors that lead each of these to success or failure, within the coordinated response as a whole, requires further research. The intention behind this Review is to compile the available information on the different aspects of the immune response, with an emphasis on those phenomena that have been studied and confirmed in the human host. For ease of comprehension, it has been subdivided in sections that cover the main humoral and cell-mediated components involved therein. However, we also intend to underline that these elements are not independent, but function intimately and concertedly. Here, we summarize years of investigation carried out to unravel the puzzling interplay between the host and the parasite.

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“…Furthermore, at very high concentrations, free IL-15 may bind to IL-15Rα on neighbouring cells for cis- or trans-presentation (5, 11). Low concentrations of IL-15 alone induce negligible NK cell activation but IL-15 is highly synergistic with other cytokines and with recall antigens such as influenza for NK cell CD25 and IFN-γ expression (12, 13).…”

Section: Introductionmentioning

confidence: 99%

IL-15 Promotes Polyfunctional NK Cell Responses to Influenza by Boosting IL-12 Production

Wagstaffe

Nielsen

Riley

et al. 2018

The Journal of Immunology

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IL-15 is a key regulator of NK cell maintenance and proliferation and synergizes with other myeloid cell–derived cytokines to enhance NK cell effector function. At low concentrations, trans-presentation of IL-15 by dendritic cells can activate NK cells, whereas at higher concentrations it can act directly on NK cells, independently of accessory cells. In this study, we investigate the potential for IL-15 to boost responses to influenza virus by promoting accessory cell function. We find that coculture of human PBMCs with inactivated whole influenza virus (A/Victoria/361/2011) in the presence of very low concentrations of IL-15 results in increased production of myeloid cell–derived cytokines, including IL-12, IFN-α2, GM-CSF, and IL-1β, and an increased frequency of polyfunctional NK cells (defined by the expression of two or more of CD107a, IFN-γ, and CD25). Neutralization experiments demonstrate that IL-15–mediated enhancement of NK cell responses is primarily dependent on IL-12 and partially dependent on IFN-αβR1 signaling. Critically, IL-15 boosted the production of IL-12 in influenza-stimulated blood myeloid dendritic cells. IL-15 costimulation also restored the ability of less-differentiated NK cells from human CMV-seropositive individuals to respond to influenza virus. These data suggest that very low concentrations of IL-15 play an important role in boosting accessory cell function to support NK cell effector functions.

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Differential IFN‐γ production by adult and neonatal blood CD56⁺ natural killer (NK) and NK‐like‐T cells in response to Trypanosoma cruzi and IL‐15

Cited by 13 publications

References 32 publications

Congenital Chagas disease as an ecological model of interactions between Trypanosoma cruzi parasites, pregnant women, placenta and fetuses

Congenital Chagas disease as an ecological model of interactions between Trypanosoma cruzi parasites, pregnant women, placenta and fetuses

The Unsolved Jigsaw Puzzle of the Immune Response in Chagas Disease

IL-15 Promotes Polyfunctional NK Cell Responses to Influenza by Boosting IL-12 Production

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Differential IFN‐γ production by adult and neonatal blood CD56+ natural killer (NK) and NK‐like‐T cells in response to Trypanosoma cruzi and IL‐15

Cited by 13 publications

References 32 publications

Congenital Chagas disease as an ecological model of interactions between Trypanosoma cruzi parasites, pregnant women, placenta and fetuses

Congenital Chagas disease as an ecological model of interactions between Trypanosoma cruzi parasites, pregnant women, placenta and fetuses

The Unsolved Jigsaw Puzzle of the Immune Response in Chagas Disease

IL-15 Promotes Polyfunctional NK Cell Responses to Influenza by Boosting IL-12 Production

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Product

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Differential IFN‐γ production by adult and neonatal blood CD56⁺ natural killer (NK) and NK‐like‐T cells in response to Trypanosoma cruzi and IL‐15