37 research outputs found

    NK cell compartment in patients with coronary heart disease

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    <p>Abstract</p> <p>Background</p> <p>Viral and bacterial infections have been considered as a risk factor for Coronary Heart Disease (CHD). NK cells, as a first line of defense against those infections, may play a role in CHD development. Thus, the main aim of our study was to determine NK cell compartment in patients with CHD undergoing coronary artery by-pass grafting.</p> <p>Results</p> <p>Ninety three patients with CHD were included into the study; the control group consisted of 49 healthy volunteers. As compared to controls, CHD patients had lower NK cytotoxic activity. CHD group had also a decreased absolute number and percentage of total NK cells and CD3-CD56dim cytotoxic NK subset. In addition, we observed tendency toward lower percentage of the CD3-CD56bright regulatory NK subset and CD3-CD56+IFN-γ+ cells in CHD patients.</p> <p>Conclusion</p> <p>These data indicate that CHD is associated with an impairment of NK cells compartment.</p

    Nutrition, diet and immunosenescence

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    Ageing is characterized by immunosenescence and the progressive decline in immunity in association with an increased frequency of infections and chronic disease. This complex process affects both the innate and adaptive immune systems with a progressive decline in most immune cell populations and defects in activation resulting in loss of function. Although host genetics and environmental factors, such as stress, exercise and diet can impact on the onset or course of immunosenescence, the mechanisms involved are largely unknown. This review focusses on identifying the most significant aspects of immunosenescence and on the evidence that nutritional intervention might delay this process, and consequently improve the quality of life of the elderly

    Baseline Levels of Influenza-Specific CD4 Memory T-Cells Affect T-Cell Responses to Influenza Vaccines

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    BACKGROUND: Factors affecting immune responses to influenza vaccines have not been studied systematically. We hypothesized that T-cell and antibody responses to the vaccines are functions of pre-existing host immunity against influenza antigens. METHODOLOGY/PRINCIPAL FINDINGS: During the 2004 and 2005 influenza seasons, we have collected data on cellular and humoral immune reactivity to influenza virus in blood samples collected before and after immunization with inactivated or live attenuated influenza vaccines in healthy children and adults. We first used cross-validated lasso regression on the 2004 dataset to identify a group of candidate baseline correlates with T-cell and antibody responses to vaccines, defined as fold-increase in influenza-specific T-cells and serum HAI titer after vaccination. The following baseline parameters were examined: percentages of influenza-reactive IFN-gamma(+) cells in T and NK cell subsets, percentages of influenza-specific memory B-cells, HAI titer, age, and type of vaccine. The candidate baseline correlates were then tested with the independent 2005 dataset. Baseline percentage of influenza-specific IFN-gamma(+) CD4 T-cells was identified as a significant correlate of CD4 and CD8 T-cell responses, with lower baseline levels associated with larger T-cell responses. Baseline HAI titer and vaccine type were identified as significant correlates for HAI response, with lower baseline levels and the inactivated vaccine associated with larger HAI responses. Previously we reported that baseline levels of CD56(dim) NK reactivity against influenza virus inversely correlated with the immediate T-cell response to vaccination, and that NK reactivity induced by influenza virus depended on IL-2 produced by influenza-specific memory T-cells. Taken together these results suggest a novel mechanism for the homeostasis of virus-specific T-cells, which involves interaction between memory helper T-cells, CD56(dim) NK and DC. SIGNIFICANCE: These results demonstrate that assessment of baseline biomarkers may predict immunologic outcome of influenza vaccination and may reveal some of the mechanisms responsible for variable immune responses following vaccination and natural infection

    NK cells in children with acute lymphoblastic leukemia and non-Hodgkin lymphoma after cessation of intensive chemotherapy

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    Intensive, combination chemotherapy for malignant diseases causes a profound immunosuppression, which persists for the whole treatment period and after its completion. Impairment of the NK cells status may increase the risk of severe, disseminated infections and cancer. The aim of the study was the investigation of recovery of NK cells after cessation of intensive chemotherapy in children with acute lymphoblastic leukemia (ALL) and non-Hodgkin lymphoma (NHL). The number of CD3 - CD16+CD56+ cells in peripheral blood and NK cell cytotoxic activity were assessed in 23 children with ALL and 7 children with NHL at 2 weeks and 12 months after the cessation of intensive chemotherapy and in 15 healthy subjects. Absolute leukocyte, lymphocyte and NK cell counts and the percentage of NK cells in children with ALL were significantly lower than in control subjects both at 2 weeks and 12 months after intensive treatment. Additionally, the absolute numbers of leukocytes and lymphocytes decreased significantly after 12 months of observations in comparison to the initial time-point. In children with non-Hodgkin lymphoma at 2 weeks and 12 months after intensive treatment only absolute lymphocyte counts were significantly lower than values in healthy children. The absolute number, the percentage and cytotoxic activity of NK cells were comparable with values in the control group both at the initial and at the last time-point. The occurrence of infections during the 12 months of observations in patients with ALL were higher than in children with NHL and as many as eight of them were hospitalized because of severe infections. The differences between the ALL and NHL patients may be connected with the milder immunosuppressive effect of chemotherapy in the non-Hodgkin lymphoma since the children recovered from acute lymphoblastic leukemia remain with persistent defect of NK cells. It is then recommended that ALL children should be supervised with respect to an increased susceptibility to infections

    Changes in number of NK cells after one year from coronary artery bypass graft

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    Natural Killer cells (NK cells) are components of nonspecific immune response involved in the defense against viral and bacterial infections. Basing on the CD56 cell surface antigen density human NK cells may be divided into two distinct subpopulations: CD56dim - "cytotoxic subset" and CD56bright - "regulatory subset". Our previous work revealed that coronary heart disease (CHD) patients are characterized by a reduction in absolute values and percentage of the CD3-CD56dim and CD3-CD56+ cells. CHD is inflammation dependent disease. Therefore we decided to estimate NK cells status in CHD patients after one year from coronary artery bypass graft (CABG). This procedure improves the heart and vascular status in patients and also remove inflammatory burden. Blood was collected from eighty five patients from the Clinic of Cardiosurgery of the Medical University of Gdańsk before CABG. Blood from eleven CHD patients was examined ones more after one year from CABG. Seventy seven people, of similar age, with excluded coronary heart disease were enrolled into the study as a control group. Percentage of the CD3-CD56+, CD3-CD56dim and CD3-CD56bright cells were analyzed in all samples by flow cytometry. Before CABG blood of the CHD patients was characterized by a low percentage of the CD3-CD56+ and CD3-CD56dim subsets in comparison to control group. However when number of cells were analyzed within one year after CABG we observed a rise of the CD3-CD56+ and CD3-CD56dim cells percentage. The increase of cell percentage was relevant when data were compared to control group and to the results obtained from CHD group before CABG. It may be concluded that a lower NK cells number in CHD is a consequence of inflammation and further that this number may be treated as marker of inflammation
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