Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)‐associated coronavirus infection
Identifieur interne : 004C66 ( Main/Exploration ); précédent : 004C65; suivant : 004C67Autoantibodies against human epithelial cells and endothelial cells after severe acute respiratory syndrome (SARS)‐associated coronavirus infection
Auteurs : Yao-Hsu Yang [Taïwan] ; Yu-Hui Huang [Taïwan] ; Ya-Hui Chuang [Taïwan] ; Chung-Min Peng [Taïwan] ; Li-Chieh Wang [Taïwan] ; Yu-Tsan Lin [Taïwan] ; Bor-Luen Chiang [Taïwan]Source :
- Journal of Medical Virology [ 0146-6615 ] ; 2005-09.
Descripteurs français
- KwdFr :
- Adulte, Anticorps antiviraux (sang), Autoanticorps (pharmacologie), Cellules endothéliales (), Cellules épithéliales (), Humains, Immunoglobuline A (sang), Immunoglobuline G (sang), Immunoglobuline M (sang), Lignée cellulaire, Protéines nucléocapside (immunologie), Syndrome respiratoire aigu sévère (immunologie), Test ELISA, Virus du SRAS (immunologie).
- MESH :
- immunologie : Protéines nucléocapside, Syndrome respiratoire aigu sévère, Virus du SRAS.
- pharmacologie : Autoanticorps.
- sang : Anticorps antiviraux, Immunoglobuline A, Immunoglobuline G, Immunoglobuline M.
- Pascal (Inist)
- MESH :
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Adult, Antibodies, Viral (blood), Autoantibodies (pharmacology), Autoantibody, Autoimmunity, Cell Line, Cytotoxicity, Endothelial Cells (drug effects), Endothelial cell, Enzyme-Linked Immunosorbent Assay, Epithelial Cells (drug effects), Epithelial cell, Human, Humans, Immunoglobulin A (blood), Immunoglobulin G (blood), Immunoglobulin M (blood), Nucleocapsid Proteins (immunology), SARS Virus (immunology), Severe Acute Respiratory Syndrome (immunology), Severe acute respiratory syndrome, Severe acute respiratory syndrome virus.
- MESH :
- chemical , blood : Antibodies, Viral, Immunoglobulin A, Immunoglobulin G, Immunoglobulin M.
- chemical , immunology : Nucleocapsid Proteins.
- chemical , pharmacology : Autoantibodies.
- drug effects : Endothelial Cells, Epithelial Cells.
- immunology : SARS Virus, Severe Acute Respiratory Syndrome.
- Teeft :
- Adult, Aeca, Aepca, Antibody, Assay, Autoantibody, Cell Line, Cell antibodies, Chan, Clin, Coronavirus, Cytotoxicity, Cytotoxicity index, Elisa, Endothelial, Endothelial cells, Enzyme-Linked Immunosorbent Assay, Epithelial, Epithelial cells, Healthy controls, Hpec, Human epithelial cells, Human umbilical venous, Humans, Huvec, Immunoglobulin, Indirect staining, National taiwan university hospital, Necrotizing pneumonia, Nucleocapsid protein, Peiris, Respiratory syndrome, Room temperature, Sars, Sars patients, Serum levels, Serum samples, Streptococcal necrotizing pneumonia, Syndrome, Systemic vasculitis, Test medium, Ulcerative colitis, Wang.
Abstract
The severe acute respiratory syndrome (SARS) is caused by infection with the SARS‐associated coronavirus (SARS‐CoV) and characterized by severe pulmonary inflammation and fibrosis. In this study, the development of autoantibodies against human epithelial cells and endothelial cells in patients with SARS at different time periods (the first week: phase I, 1 month after the disease onset: phase II/phase III) were investigated. Antibodies in sera of patients and healthy controls against: (1) A549 human pulmonary epithelial cell‐line, (2) human umbilical venous endothelial cells (HUVEC), (3) primary human pulmonary endothelial cells (HPEC) were detected by cell‐based ELISA and indirect immunofluorescence staining. The results revealed that serum levels of IgG anti‐A549 cells antibodies, IgG anti‐HUVEC antibodies, and IgM anti‐HPEC antibodies were significantly higher in SARS patients at phase II/phase III than those in healthy controls. Sera from SARS patients at phase II/phase III could mediate complement dependent cytotoxicity against some A549 cells and HPEC. It is concluded that some autoantibodies against human epithelial cells and endothelial cells would be developed after SARS‐CoV infection and this phenomenon may indicate post‐infectious cellular injury and also induce SARS‐induced immunopathology. J. Med. Virol. 77:1–7, 2005. © 2005 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jmv.20407
Affiliations:
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Le document en format XML
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level="j" type="main">Journal of Medical Virology</title><title level="j" type="alt">JOURNAL OF MEDICAL VIROLOGY</title><idno type="ISSN">0146-6615</idno><idno type="eISSN">1096-9071</idno><imprint><biblScope unit="vol">77</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="1">1</biblScope><biblScope unit="page" to="7">7</biblScope><biblScope unit="page-count">7</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2005-09">2005-09</date></imprint><idno type="ISSN">0146-6615</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0146-6615</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Antibodies, Viral (blood)</term><term>Autoantibodies (pharmacology)</term><term>Autoantibody</term><term>Autoimmunity</term><term>Cell Line</term><term>Cytotoxicity</term><term>Endothelial Cells (drug 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(immunologie)</term><term>Syndrome respiratoire aigu sévère (immunologie)</term><term>Test ELISA</term><term>Virus du SRAS (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Antibodies, Viral</term><term>Immunoglobulin A</term><term>Immunoglobulin G</term><term>Immunoglobulin M</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Nucleocapsid Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Autoantibodies</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Endothelial Cells</term><term>Epithelial Cells</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Protéines nucléocapside</term><term>Syndrome respiratoire aigu sévère</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>SARS Virus</term><term>Severe Acute Respiratory Syndrome</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Autoanticorps</term></keywords><keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Anticorps antiviraux</term><term>Immunoglobuline A</term><term>Immunoglobuline G</term><term>Immunoglobuline M</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Autoanticorps</term><term>Autoimmunité</term><term>Cellule endothéliale</term><term>Cellule épithéliale</term><term>Cytotoxicité</term><term>Homme</term><term>Syndrome respiratoire aigu sévère</term><term>Virus syndrome respiratoire aigu sévère</term></keywords><keywords scheme="Teeft" xml:lang="en"><term>Adult</term><term>Aeca</term><term>Aepca</term><term>Antibody</term><term>Assay</term><term>Autoantibody</term><term>Cell Line</term><term>Cell antibodies</term><term>Chan</term><term>Clin</term><term>Coronavirus</term><term>Cytotoxicity</term><term>Cytotoxicity 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épithéliales</term><term>Humains</term><term>Lignée cellulaire</term><term>Test ELISA</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The severe acute respiratory syndrome (SARS) is caused by infection with the SARS‐associated coronavirus (SARS‐CoV) and characterized by severe pulmonary inflammation and fibrosis. In this study, the development of autoantibodies against human epithelial cells and endothelial cells in patients with SARS at different time periods (the first week: phase I, 1 month after the disease onset: phase II/phase III) were investigated. Antibodies in sera of patients and healthy controls against: (1) A549 human pulmonary epithelial cell‐line, (2) human umbilical venous endothelial cells (HUVEC), (3) primary human pulmonary endothelial cells (HPEC) were detected by cell‐based ELISA and indirect immunofluorescence staining. The results revealed that serum levels of IgG anti‐A549 cells antibodies, IgG anti‐HUVEC antibodies, and IgM anti‐HPEC antibodies were significantly higher in SARS patients at phase II/phase III than those in healthy controls. Sera from SARS patients at phase II/phase III could mediate complement dependent cytotoxicity against some A549 cells and HPEC. It is concluded that some autoantibodies against human epithelial cells and endothelial cells would be developed after SARS‐CoV infection and this phenomenon may indicate post‐infectious cellular injury and also induce SARS‐induced immunopathology. J. Med. Virol. 77:1–7, 2005. © 2005 Wiley‐Liss, Inc.</div></front></TEI><affiliations><list><country><li>Taïwan</li></country></list><tree><country name="Taïwan"><noRegion><name sortKey="Yang, Yao Su" sort="Yang, Yao Su" uniqKey="Yang Y" first="Yao-Hsu" last="Yang">Yao-Hsu Yang</name></noRegion><name sortKey="Chiang, Bor Uen" sort="Chiang, Bor Uen" uniqKey="Chiang B" first="Bor-Luen" last="Chiang">Bor-Luen Chiang</name><name sortKey="Chiang, Bor Uen" sort="Chiang, Bor Uen" uniqKey="Chiang B" first="Bor-Luen" last="Chiang">Bor-Luen Chiang</name><name sortKey="Chiang, Bor Uen" sort="Chiang, Bor Uen" uniqKey="Chiang B" first="Bor-Luen" last="Chiang">Bor-Luen Chiang</name><name sortKey="Chuang, Ya Ui" sort="Chuang, Ya Ui" uniqKey="Chuang Y" first="Ya-Hui" last="Chuang">Ya-Hui Chuang</name><name sortKey="Huang, Yu Ui" sort="Huang, Yu Ui" uniqKey="Huang Y" first="Yu-Hui" last="Huang">Yu-Hui Huang</name><name sortKey="Lin, Yu San" sort="Lin, Yu San" uniqKey="Lin Y" first="Yu-Tsan" last="Lin">Yu-Tsan Lin</name><name sortKey="Peng, Chung In" sort="Peng, Chung In" uniqKey="Peng C" first="Chung-Min" last="Peng">Chung-Min Peng</name><name sortKey="Wang, Li Hieh" sort="Wang, Li Hieh" uniqKey="Wang L" first="Li-Chieh" last="Wang">Li-Chieh Wang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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