Antibody to severe acute respiratory syndrome (SARS)-associated coronavirus spike protein domain 2 cross-reacts with lung epithelial cells and causes cytotoxicity
Identifieur interne : 000354 ( PascalFrancis/Curation ); précédent : 000353; suivant : 000355Antibody 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 :
- Clinical and experimental immunology : (Print) [ 0009-9104 ] ; 2005.
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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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<front><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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<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>
</record>
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