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  • 1985-1989  (2)
  • 1988  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 66 (1988), S. 865-872 
    ISSN: 1432-1440
    Keywords: Hepatitis B-vaccination ; Dialysis patients ; Immune deficiency ; Monocyte function ; Hepatitis B-Impfung ; Dialyse-Patienten ; Sekundärer Immundefekt ; Monozytendefekt
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die aktive Hepatitis-B-Impfung führt bei Gesunden in über 95%, bei Dialysepatienten nur in ca. 60% zur Bildung protektiver anti-HBs-Antikörper. In vitro geht der Non-Responder-Status mit einer gestörten Monozytenfunktion einher, die eine mangelhafte Interleukin-2-Produktion nach sich zieht. Gleichzeitig findet sich eine vermehrte Expression funktioneller Interleukin-2-Rezeptoren. Exogen zugeführtes Interleukin-2 normalisiert daher bereits in niedriger Dosierung die vorher verminderte proliferative Antwort von Non-Responder-Lymphozyten in vitro. Außerdem läßt sich der Non-Responder-Status von Dialysepatienten in vivo beheben, wenn zur Standard-Impfung mit 40 µg Hepatitis B-Vakzine zusätzlich eine niedrige Interleukin-2-Dosis (2,5 × 105 Einheiten) lokal appliziert wird.
    Notes: Summary In dialysis patients the immune response to hepatitis B-vaccination is greatly impaired. In vitro the non-responders show a failure of the monocytes to support the process of primary T-cell activation. This defect results in a lack of interleukin 2-production and an enhanced sensitivity of the interleukin-2 receptor system. Addition of low doses of interleukin-2 fully reconstitutes the deficient immune response in vitro. Furthermore, the local application of low dose interleukin-2 during a standard vaccination with 40 µg hepatitis B-vaccine normalizes the non-responder state in vivo.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0851
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The natural killer (NK) cell activity of mice in the peritoneal cavity is very low or undetectable and testing peritoneal NK cells is a useful model for studying the influence of activating substances upon local injection. Injection of tumor necrosis factor (TNF) at doses of 10–200 ng caused a marked activation of NK cell activity which was maximal after 24 h and declined rapidly on day 2. A similar effect was observed when interferons alpha and beta were injected, and there were additive results when interferon was injected together with TNF. The NK cell nature of the effector cells activated by TNF was substantiated by the finding that previous injection with anti-asialo GM 1 antibody prevented activation. Interferon could not be detected in the peritoneal wash fluid after injection of TNF suggesting interferon-independent activation. In further experiments after i.p. injection of TNF peritoneal exudate cells (PECs) only killed YAC-1 targets in a 4-h assay. There was no additional killing in an 18-h assay towards neither YAC-1 cells or P815 cells, suggesting that macrophages were not involved. Furthermore TNF was also active in vitro by activating NK cells in isolated human peripheral blood cells. However in the PECs stimulated in vitro no significant induction of cytotoxic capacities by TNF was measured. Our data suggest that the action of TNF is not restricted to the lysis of tumor cells but can also induce immunological properties in the host defense against virus infections and neoplasms.
    Type of Medium: Electronic Resource
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