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Antibody to severe acute respiratory syndrome (SARS)-associated coronavirus spike protein domain 2 cross-reacts with lung epithelial cells and causes cytotoxicity

Identifieur interne : 000705 ( PascalFrancis/Checkpoint ); précédent : 000704; suivant : 000706

Antibody to severe acute respiratory syndrome (SARS)-associated coronavirus spike protein domain 2 cross-reacts with lung epithelial cells and causes cytotoxicity

Auteurs : Y. S. Lin [Taïwan] ; C. F. Lin [Taïwan] ; Y. T. Fang [Taïwan] ; Y. M. Kuo [Taïwan] ; P. C. Liao [Taïwan] ; T. M. Yeh [Taïwan] ; K. Y. Hwa [Taïwan] ; C. C. K. Shieh [Taïwan] ; J. H. Yen [Taïwan] ; H. J. Wang [Taïwan] ; I. J. Su [Taïwan] ; H. Y. Lei [Taïwan]

Source :

RBID : Pascal:05-0334001

Descripteurs français

English descriptors

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-γ 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.


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Pascal:05-0334001

Le document en format XML

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<div type="abstract" xml:lang="en">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-γ 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.</div>
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<s1>LIAO (P. C.)</s1>
</fA11>
<fA11 i1="06" i2="1">
<s1>YEH (T. M.)</s1>
</fA11>
<fA11 i1="07" i2="1">
<s1>HWA (K. Y.)</s1>
</fA11>
<fA11 i1="08" i2="1">
<s1>SHIEH (C. C. K.)</s1>
</fA11>
<fA11 i1="09" i2="1">
<s1>YEN (J. H.)</s1>
</fA11>
<fA11 i1="10" i2="1">
<s1>WANG (H. J.)</s1>
</fA11>
<fA11 i1="11" i2="1">
<s1>SU (I. J.)</s1>
</fA11>
<fA11 i1="12" i2="1">
<s1>LEI (H. Y.)</s1>
</fA11>
<fA14 i1="01">
<s1>Department of Microbiology and Immunology, National Cheng Kung University Medical College</s1>
<s2>Tainan</s2>
<s3>TWN</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>12 aut.</sZ>
</fA14>
<fA14 i1="02">
<s1>Department of Cell Biology and Anatomy, National Cheng Kung University Medical College</s1>
<s2>Tainan</s2>
<s3>TWN</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="03">
<s1>Departmnt of Environmental and Occupational Health, National Cheng Kung University Medical College</s1>
<s2>Tainan</s2>
<s3>TWN</s3>
<sZ>5 aut.</sZ>
<sZ>9 aut.</sZ>
</fA14>
<fA14 i1="04">
<s1>Department of Medical Technology, National Cheng Kung University Medical College</s1>
<s2>Tainan</s2>
<s3>TWN</s3>
<sZ>6 aut.</sZ>
<sZ>7 aut.</sZ>
</fA14>
<fA14 i1="05">
<s1>Department of Paediatrics, National Cheng Kung University Medical College</s1>
<s2>Tainan</s2>
<s3>TWN</s3>
<sZ>8 aut.</sZ>
</fA14>
<fA14 i1="06">
<s1>Division of Clinical Research, National Health Research Institutes</s1>
<s2>Tainan</s2>
<s3>TWN</s3>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="07">
<s1>Centre for Disease Control, Department of Health</s1>
<s2>Taipei</s2>
<s3>TWN</s3>
<sZ>11 aut.</sZ>
</fA14>
<fA14 i1="08">
<s1>ScinoPharm Biotech Ltd</s1>
<s2>Tainan</s2>
<s3>TWN</s3>
</fA14>
<fA20>
<s1>500-508</s1>
</fA20>
<fA21>
<s1>2005</s1>
</fA21>
<fA23 i1="01">
<s0>ENG</s0>
</fA23>
<fA43 i1="01">
<s1>INIST</s1>
<s2>12690</s2>
<s5>354000137997970150</s5>
</fA43>
<fA44>
<s0>0000</s0>
<s1>© 2005 INIST-CNRS. All rights reserved.</s1>
</fA44>
<fA45>
<s0>41 ref.</s0>
</fA45>
<fA47 i1="01" i2="1">
<s0>05-0334001</s0>
</fA47>
<fA60>
<s1>P</s1>
</fA60>
<fA61>
<s0>A</s0>
</fA61>
<fA64 i1="01" i2="1">
<s0>Clinical and experimental immunology : (Print)</s0>
</fA64>
<fA66 i1="01">
<s0>GBR</s0>
</fA66>
<fC01 i1="01" l="ENG">
<s0>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-γ 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.</s0>
</fC01>
<fC02 i1="01" i2="X">
<s0>002B06</s0>
</fC02>
<fC02 i1="02" i2="X">
<s0>002A06</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE">
<s0>Syndrome respiratoire aigu sévère</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG">
<s0>Severe acute respiratory syndrome</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA">
<s0>Síndrome respiratorio agudo severo</s0>
<s2>NM</s2>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE">
<s0>Anticorps</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG">
<s0>Antibody</s0>
<s5>02</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA">
<s0>Anticuerpo</s0>
<s5>02</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE">
<s0>Coronavirus</s0>
<s2>NW</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG">
<s0>Coronavirus</s0>
<s2>NW</s2>
<s5>03</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA">
<s0>Coronavirus</s0>
<s2>NW</s2>
<s5>03</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE">
<s0>Autoimmunité</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG">
<s0>Autoimmunity</s0>
<s5>04</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA">
<s0>Autoinmunidad</s0>
<s5>04</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE">
<s0>Protéine</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG">
<s0>Protein</s0>
<s5>05</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA">
<s0>Proteína</s0>
<s5>05</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE">
<s0>Cellule épithéliale</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG">
<s0>Epithelial cell</s0>
<s5>06</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA">
<s0>Célula epitelial</s0>
<s5>06</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE">
<s0>Cytotoxicité</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG">
<s0>Cytotoxicity</s0>
<s5>08</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA">
<s0>Citotoxicidad</s0>
<s5>08</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE">
<s0>Autoanticorps</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG">
<s0>Autoantibody</s0>
<s5>09</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA">
<s0>Autoanticuerpo</s0>
<s5>09</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE">
<s0>Virose</s0>
</fC07>
<fC07 i1="01" i2="X" l="ENG">
<s0>Viral disease</s0>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Virosis</s0>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Infection</s0>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Infection</s0>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Infección</s0>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Coronaviridae</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Nidovirales</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Virus</s0>
<s2>NW</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Poumon pathologie</s0>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Lung disease</s0>
<s5>37</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Pulmón patología</s0>
<s5>37</s5>
</fC07>
<fC07 i1="07" i2="X" l="FRE">
<s0>Immunologie</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="ENG">
<s0>Immunology</s0>
<s5>38</s5>
</fC07>
<fC07 i1="07" i2="X" l="SPA">
<s0>Inmunología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="08" i2="X" l="FRE">
<s0>Immunopathologie</s0>
<s5>39</s5>
</fC07>
<fC07 i1="08" i2="X" l="ENG">
<s0>Immunopathology</s0>
<s5>39</s5>
</fC07>
<fC07 i1="08" i2="X" l="SPA">
<s0>Inmunopatología</s0>
<s5>39</s5>
</fC07>
<fC07 i1="09" i2="X" l="FRE">
<s0>Appareil respiratoire pathologie</s0>
<s5>40</s5>
</fC07>
<fC07 i1="09" i2="X" l="ENG">
<s0>Respiratory disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="09" i2="X" l="SPA">
<s0>Aparato respiratorio patología</s0>
<s5>40</s5>
</fC07>
<fN21>
<s1>234</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
<affiliations>
<list>
<country>
<li>Taïwan</li>
</country>
</list>
<tree>
<country name="Taïwan">
<noRegion>
<name sortKey="Lin, Y S" sort="Lin, Y S" uniqKey="Lin Y" first="Y. S." last="Lin">Y. S. Lin</name>
</noRegion>
<name sortKey="Fang, Y T" sort="Fang, Y T" uniqKey="Fang Y" first="Y. T." last="Fang">Y. T. Fang</name>
<name sortKey="Hwa, K Y" sort="Hwa, K Y" uniqKey="Hwa K" first="K. Y." last="Hwa">K. Y. Hwa</name>
<name sortKey="Kuo, Y M" sort="Kuo, Y M" uniqKey="Kuo Y" first="Y. M." last="Kuo">Y. M. Kuo</name>
<name sortKey="Lei, H Y" sort="Lei, H Y" uniqKey="Lei H" first="H. Y." last="Lei">H. Y. Lei</name>
<name sortKey="Liao, P C" sort="Liao, P C" uniqKey="Liao P" first="P. C." last="Liao">P. C. Liao</name>
<name sortKey="Lin, C F" sort="Lin, C F" uniqKey="Lin C" first="C. F." last="Lin">C. F. Lin</name>
<name sortKey="Lin, Y S" sort="Lin, Y S" uniqKey="Lin Y" first="Y. S." last="Lin">Y. S. Lin</name>
<name sortKey="Shieh, C C K" sort="Shieh, C C K" uniqKey="Shieh C" first="C. C. K." last="Shieh">C. C. K. Shieh</name>
<name sortKey="Shieh, C C K" sort="Shieh, C C K" uniqKey="Shieh C" first="C. C. K." last="Shieh">C. C. K. Shieh</name>
<name sortKey="Su, I J" sort="Su, I J" uniqKey="Su I" first="I. J." last="Su">I. J. Su</name>
<name sortKey="Su, I J" sort="Su, I J" uniqKey="Su I" first="I. J." last="Su">I. J. Su</name>
<name sortKey="Wang, H J" sort="Wang, H J" uniqKey="Wang H" first="H. J." last="Wang">H. J. Wang</name>
<name sortKey="Yeh, T M" sort="Yeh, T M" uniqKey="Yeh T" first="T. M." last="Yeh">T. M. Yeh</name>
<name sortKey="Yen, J H" sort="Yen, J H" uniqKey="Yen J" first="J. H." last="Yen">J. H. Yen</name>
</country>
</tree>
</affiliations>
</record>

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   |wiki=    Sante
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   |texte=   Antibody to severe acute respiratory syndrome (SARS)-associated coronavirus spike protein domain 2 cross-reacts with lung epithelial cells and causes cytotoxicity
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