國家衛生研究院 NHRI:Item 3990099045/2106
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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/2106


    Title: Antibody to severe acute respiratory syndrome (SARS)-associated coronavirus spike protein domain 2 cross-reacts with lung epithelial cells and causes cytotoxicity
    Authors: Lin, YS;Lin, CF;Fang, YT;Kuo, YM;Liao, PC;Yeh, TM;Hwa, KY;Shieh, CCK;Yen, JH;Wang, HJ;Su, IJ;Lei, HY
    Contributors: Division of Clinical Research
    Abstract: Both viral effect and immune-mediated mechanism are involved in the pathogenesis of severe acute respiratory syndrome-associated coronavirus (SARS-CoV) infection. In this study, we showed that in SARS patient sera there were autoantibodies (autoAbs) that reacted with A549 cells, the type-2 pneumocytes, and that these autoAbs were mainly IgG. The autoAbs were detectable 20 days after fever onset. Tests of non-SARS-pneumonia patients did not show the same autoAb production as in SARS patients. After sera IgG bound to A549 cells, cytotoxicity was induced. Cell cytotoxicity and the anti-epithelial cell IgG level were positively correlated. Preabsorption and binding assays indicated the existence of cross-reactive epitopes on SARS-CoV spike protein domain 2 (S2). Furthermore, treatment of A549 cells with anti-S2 Abs and IFN-gamma resulted in an increase in the adherence of human peripheral blood mononuclear cells to these epithelial cells. Taken together, we have demonstrated that the anti-S2 Abs in SARS patient sera cause cytotoxic injury as well as enhance immune cell adhesion to epithelial cells. The onset of autoimmune responses in SARS-CoV infection may be implicated in SARS pathogenesis.
    Keywords: Immunology
    Date: 2005-09
    Relation: Clinical and Experimental Immunology. 2005 Sep;141(3):500-508.
    Link to: http://dx.doi.org/10.1111/j.1365-2249.2005.02864.x
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0009-9104&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000230628300015
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=23044469875
    Appears in Collections:[Ih-Jen Su(2002-2015)] Periodical Articles

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