Production of interferon-γ by natural killer cells and aging in chronic human schistosomiasis

BACKGROUNG: Aging is associated with several alterations in the phenotype, repertoire and activation status of lymphocytes as well as in the cytokine profile produced by these cells. As a lifelong condition, chronic parasitic diseases such as human schistosomiasis overlaps with the aging process and no systematic study has yet addressed the changes in immune response during infection withSchistosoma mansoniin older individuals.Aim: Herein we study the influence of immunological alterations brought about by senescence in the course of schistosomiasis.Materials and methods: Individuals 10-95 years of age, from both sexes, from an endemic area forS. mansoniinfection were matched by intensity of infection as measured by egg counts. We analyzed, as a parameter, cytokine expression by lymphocytes and natural killer cells afterin vitrostimulation with soluble egg antigen and soluble worm antigen using flow cytometry.Results: We demonstrated that the frequency of CD16+interferon-γ (IFN-γ)+natural killer cells in negative individuals over the age of 70 years is significantly higher than in positive individuals afterin vitrostimulation withS. mansoniantigen extracts. The frequency of these cells is increased in all individuals over the age of 50 years and only declines in positive individuals after 70 years of age. Analysis of either CD4?or CD8?cells after antigen stimulation show no significant increase in frequency of IFN-γ in negative or in positive individuals of this age group, suggesting that the effect on CD16+cells is not T-cell dependent.Conclusion: Since production of IFN-γ has been related to resistance to schistosome infection, our data suggest that age-associated changes in CD16+cells may play a role in controlling infection intensity in the elderly inS. mansoniendemic areas of Brazil.

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Prokaryotic Expression and Anti-IBDV Activity of Chicken Interleukin-18 and Interferon-γ

Cytogenetic and Genome Research ◽

10.1159/000481522 ◽

2017 ◽

Vol 153 (1) ◽

pp. 36-45 ◽

Cited By ~ 3

Author(s):

Baifen Song ◽

Xiaoting Li ◽

Jinzhu Ma ◽

Liquan Yu ◽

Zhenyue Feng ◽

...

Keyword(s):

Natural Killer Cells ◽

Natural Killer ◽

Prokaryotic Expression ◽

Interferon Γ ◽

Fibroblast Cells ◽

Killer Cells ◽

Chicken Embryonic Fibroblast ◽

Prokaryotic Expression Vector ◽

Ifn Γ ◽

Embryonic Fibroblast

Interferon-γ (IFN-γ), a cytokine produced by activated natural killer cells and T lymphocytes, is an important regulator of innate and adaptive immunity. Interleukin (IL)-18, also known as IFN-γ-inducing factor, is a cytokine that induces T and natural killer cells to produce IFN-γ. In this study, the chicken IL-18 (ChIL-18) and chicken IFN-γ (ChIFN-γ) genes were inserted into the pET28a prokaryotic expression vector, resulting in pET28a-IL-18 and pET28a-IFN-γ, respectively. These plasmids were transformed into Escherichia coli strain BL21, and the ChIL-18 and ChIFN-γ proteins were expressed and purified. To determine their antiviral activities, 200 ng/mL of ChIL-18 and/or ChIFN-γ were inoculated into chicken embryonic fibroblast cells. After 24 h, one 50% tissue culture infective dose (TCID50) of infectious bursal disease virus (IBDV) was inoculated into the chicken embryonic fibroblast cells. The results showed that the antiviral effect of ChIL-18 and ChIFN-γ in combination was better than that of ChIL-18 or ChIFN-γ alone. Next, 14-day-old chicken were injected with 200 µg of ChIL-18 and/or ChIFN-γ and then were challenged with 103 TCID50 of IBDV via intraperitoneal injection. The results showed that the proliferation of IBDV was inhibited by the injection of the recombinant proteins, especially the combination of ChIL-18 and ChIFN-γ, as evidenced by cytokine detection, quantitative PCR, and pathology analyses. These results indicate that ChIL-18 and ChIFN-γ could inhibit IBDV infection and the combination of ChIL-18 and ChIFN-γ has a better inhibitory effect than either cytokine alone.

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Interferon‐γ Production by Human T Cells and Natural Killer Cells In Vitro in Response to Antigens from the Two Intracellular Pathogens Mycobacterium tuberculosis and Leishmania major

Scandinavian Journal of Immunology ◽

10.1046/j.1365-3083.1997.d01-154.x ◽

1997 ◽

Vol 46 (5) ◽

pp. 495-499 ◽

Cited By ~ 18

Author(s):

K. KEMP ◽

L. HVIID ◽

A. KHARAZMI ◽

M. KEMP

Keyword(s):

T Cells ◽

Mycobacterium Tuberculosis ◽

Natural Killer Cells ◽

Natural Killer ◽

Leishmania Major ◽

Interferon Γ ◽

Intracellular Pathogens ◽

Killer Cells ◽

Human T Cells

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Prolactin Induces IL-2 Associated TRAIL Expression on Natural Killer Cells from Chronic Hepatitis C PatientsIn vivoandIn vitro

Endocrine Metabolic & Immune Disorders - Drug Targets ◽

10.2174/1871530319666181206125545 ◽

2019 ◽

Vol 19 (7) ◽

pp. 975-984

Author(s):

Maria L.H. Medel ◽

Gabriela G. Reyes ◽

Luz M. Porras ◽

Arturo R. Bernal ◽

Jesús S. Luna ◽

...

Keyword(s):

Viral Load ◽

Natural Killer Cells ◽

Natural Killer ◽

Mononuclear Cells ◽

Killer Cells ◽

Trail Expression ◽

Viral Loads ◽

Nkg2d Expression ◽

Ifn Γ

Background:Natural killer cells (NKC) are a major component of the innate immune response to HCV, mediating their effects through TRAIL and IFN-γ. However, their function is diminished in chronic HCV patients (HCVp). Prolactin is an immunomodulatory hormone capable of activating NKC.Objective:The study aims to explore if hyperprolactinemia can activate NKC in HCVp.Methods:We treated twelve chronic HCVp (confidence level =95%, power =80%) for 15 days with Levosulpiride plus Cimetidine to induce mild hyperprolactinemia. Before and after treatment, we determined TRAIL and NKG2D expression on peripheral blood NKC, along with cytokine profiles, viral loads and liver function. We also evaluated in vitro effects of prolactin and/or IL-2 on NKC TRAIL or NKG2D expression and IFN-γ levels on cultured blood mononuclear cells from 8 HCVp and 7 healthy controls.Results:The treatment induced mild hyperprolactinemia and increased TRAIL expression on NKC as well as the secretion of IL-1ra, IL-2, PDGF and IFN-γ. Viral loads decreased in six HCVp. IL-2 and TRAIL together explained the viral load decrease. In vitro, prolactin plus IL-2 synergized to increase TRAIL and NKG2D expression on NKC from HCVp but not in controls.Conclusion:Levosulpiride/Cimetidine treatment induced mild hyperprolactinaemia that was associated with NKC activation and Th1-type cytokine profile. Also, an increase in TRAIL and IL-2 was associated with viral load decrease. This treatment could potentially be used to reactivate NKC in HCVp.

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