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      Innate Antiviral Immunity Is Not Impaired in Patients with Chronic Renal Failure on Hemodialysis

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          Although it is well documented that chronic renal failure patients are susceptible to infectious diseases, the reason for this has not been clarified. The aim of the study was to assess the antiviral natural (innate) immunity of peripheral leukocytes in 37 hemodialysis patients and compare it with that of a of control group (70 blood donors). We investigated 16 patients with anti-hepatitis C virus (HCV) antibodies, anti-HCV(+) and 21 patients without anti-HCV antibodies, anti-HCV(–). Methods: Innate immunity was measured using the method of direct infection of peripheral blood leukocytes with indicatory VS virus. The VS virus did not replicate in leukocytes with strong innate immunity, whereas by impaired immunity the virus multiplied to high titer. Results: Patients on hemodialysis expressed the same levels of nonspecific antiviral immunity as the control group. We found complete, partial or deficient of innate immunity respectively in 33, 52.5, 14.5% of anti-HCV(–) patients, 43, 43 and 14% of anti-HCV(+) patients, and 44, 40 and 16% of controls. Conclusions: Innate antiviral immunity was not impaired (disturbed) in chronic HD patients. The categories of innate immunity disposition in dialysis patients and the healthy population did not differ.

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          The immune system in end-stage renal disease.

          Patients with end-stage renal disease present with an immunodeficient state paradoxically coexisting with signs of activation of immune system cells and that is accentuated rather than corrected by replacement dialysis therapy. The mechanisms of this immune system dysregulation presently under consideration are a reduced bioavailability of interleukin-2 secondary to its overconsumption by activated T cells; a downregulation of phagocyte adhesion molecules and opsonin receptors following their overexpression during dialysis with complement-activating membranes; an increased production of the cytokines interleukin-1, tumor necrosis factor-alpha, and interleukin-6 by activated monocytes and of soluble CD23 by B lymphocytes; and last, but far from least, the presence of uremic toxins. Perspectives of research are aimed at elucidating the respective role of the T helper cell subpopulations (Th-1 and Th-2) and the influence of the progression of chronic renal failure on the naturally occurring cytokine inhibitors, with the hope of better defining the rationale of strategies of immunomodulation that could be beneficial to patients with end-stage renal disease.
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            Antiviral Nonspecific Immunity of Human Placenta at Term: Possible Role of Endogenous Tumor Necrosis Factors and Interferons

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              Natural cytotoxicity and antibody-dependent cellular cytotoxicity (ADCC) is not impaired in patients suffering from chronic hepatitis C


                Author and article information

                Nephron Clin Pract
                Nephron Clinical Practice
                S. Karger AG
                December 2005
                30 August 2005
                : 101
                : 4
                : c207-c210
                aLaboratory of Virology, Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, and bDepartment of Nephrology and Transplant Medicine, University School of Medicine, Wroclaw, Poland
                87941 Nephron Clin Pract 2005;101:c207–c210
                © 2005 S. Karger AG, Basel

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                Figures: 2, Tables: 1, References: 12, Pages: 1
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