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Immunoregulation by natural killer cells
Authors:L V Abruzzo  C A Mullen  D A Rowley
Affiliation:1. Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, NY, USA;2. Center for Biomedical Imaging at Clinical and Translational Science Institute, University of Buffalo, State University of New York, NY, USA;3. Department of Pharmaceutical Sciences, State University of New York, Buffalo, NY, USA;4. Jacobs Multiple Sclerosis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, NY, USA;1. Amsterdam UMC location University of Amsterdam, Department of Intensive Care Medicine, Meibergdreef 9, Amsterdam, the Netherlands;2. Amsterdam UMC Location University of Amsterdam, Laboratory of Experimental Intensive Care and Anesthesiology (L.E.I.C.A.), Amsterdam, the Netherlands;3. Amsterdam UMC location University of Amsterdam, Department of Neurology, Meibergdreef 9, Amsterdam, the Netherlands;4. Amsterdam Neuroscience, Amsterdam, the Netherlands;5. Amsterdam UMC location University of Amsterdam, Center for Experimental and Molecular Medicine, Amsterdam, the Netherlands
Abstract:Polyinosinic-polycytidilic acid (poly (I:C], a synthetic analog of viral double-stranded RNA (dsRNA), activates natural killer (NK) cells and inhibits induction or promotes termination of the primary IgM response in vivo. Suppression of responses was reproduced in vivo by interferons (IFN) which activate NK cells and in vitro by cells enriched for NK cells. The likelihood that NK cells may be involved in the normal regulation of IgM responses is supported by the following observations: immunization itself induces NK activity at times appropriate to account for termination, NK cells activated by immunization suppress in vitro, mice with high NK activity induced by immunization with one antigen have reduced responses to immunization with a second antigen, and mice with induced loss of NK activity fail to down-regulate IgM antibody responses normally.
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