Annexin A2 on lung epithelial cell surface is recognized by severe acute respiratory syndrome-associated coronavirus spike domain 2 antibodies.
Identifieur interne : 001714 ( PubMed/Checkpoint ); précédent : 001713; suivant : 001715Annexin A2 on lung epithelial cell surface is recognized by severe acute respiratory syndrome-associated coronavirus spike domain 2 antibodies.
Auteurs : Yi-Ting Fang [Taïwan] ; Chiou-Feng Lin ; Pao-Chi Liao ; Yu-Min Kuo ; Shuying Wang ; Trai-Ming Yeh ; Chi-Chang K. Shieh ; Ih-Jen Su ; Huan-Yao Lei ; Yee-Shin LinSource :
- Molecular immunology [ 1872-9142 ] ; 2010.
Descripteurs français
- KwdFr :
- Annexine A2 (immunologie), Anticorps antiviraux (immunologie), Antiviraux (pharmacologie), Autoantigènes (immunologie), Cellules épithéliales (anatomopathologie), Cellules épithéliales (immunologie), Cellules épithéliales (virologie), Glycoprotéine de spicule des coronavirus, Glycoprotéines membranaires (immunologie), Humains, Interféron gamma (pharmacologie), Interleukine-6 (pharmacologie), Lignée cellulaire tumorale, Muqueuse respiratoire (anatomopathologie), Muqueuse respiratoire (immunologie), Muqueuse respiratoire (virologie), Protéines de l'enveloppe virale (immunologie), Réactions croisées (immunologie), Régulation positive (), Régulation positive (immunologie), Structure tertiaire des protéines, Syndrome respiratoire aigu sévère (anatomopathologie), Syndrome respiratoire aigu sévère (immunologie), Syndrome respiratoire aigu sévère (virologie), Virus du SRAS (immunologie).
- MESH :
- anatomopathologie : Cellules épithéliales, Muqueuse respiratoire, Syndrome respiratoire aigu sévère.
- immunologie : Annexine A2, Anticorps antiviraux, Autoantigènes, Cellules épithéliales, Glycoprotéines membranaires, Muqueuse respiratoire, Protéines de l'enveloppe virale, Réactions croisées, Régulation positive, Syndrome respiratoire aigu sévère, Virus du SRAS.
- pharmacologie : Antiviraux, Interféron gamma, Interleukine-6.
- virologie : Cellules épithéliales, Muqueuse respiratoire, Syndrome respiratoire aigu sévère.
- Glycoprotéine de spicule des coronavirus, Humains, Lignée cellulaire tumorale, Régulation positive, Structure tertiaire des protéines.
English descriptors
- KwdEn :
- Annexin A2 (immunology), Antibodies, Viral (immunology), Antiviral Agents (pharmacology), Autoantigens (immunology), Cell Line, Tumor, Cross Reactions (immunology), Epithelial Cells (immunology), Epithelial Cells (pathology), Epithelial Cells (virology), Humans, Interferon-gamma (pharmacology), Interleukin-6 (pharmacology), Membrane Glycoproteins (immunology), Protein Structure, Tertiary, Respiratory Mucosa (immunology), Respiratory Mucosa (pathology), Respiratory Mucosa (virology), SARS Virus (immunology), Severe Acute Respiratory Syndrome (immunology), Severe Acute Respiratory Syndrome (pathology), Severe Acute Respiratory Syndrome (virology), Spike Glycoprotein, Coronavirus, Up-Regulation (drug effects), Up-Regulation (immunology), Viral Envelope Proteins (immunology).
- MESH :
- chemical , immunology : Annexin A2, Antibodies, Viral, Autoantigens, Membrane Glycoproteins, Viral Envelope Proteins.
- chemical , pharmacology : Antiviral Agents, Interferon-gamma, Interleukin-6.
- drug effects : Up-Regulation.
- immunology : Cross Reactions, Epithelial Cells, Respiratory Mucosa, SARS Virus, Severe Acute Respiratory Syndrome, Up-Regulation.
- pathology : Epithelial Cells, Respiratory Mucosa, Severe Acute Respiratory Syndrome.
- virology : Epithelial Cells, Respiratory Mucosa, Severe Acute Respiratory Syndrome.
- Cell Line, Tumor, Humans, Protein Structure, Tertiary, Spike Glycoprotein, Coronavirus.
Abstract
Severe acute respiratory syndrome-associated coronavirus (SARS-CoV) infection causes lung failure characterized by atypical pneumonia. We previously showed that antibodies against SARS-CoV spike domain 2 (S2) in the patient sera can cross-react with human lung epithelial cells; however, the autoantigen is not yet identified. In this study, we performed proteomic studies and identified several candidate autoantigens recognized by SARS patient sera in human lung type II epithelial cell A549. Among the candidate proteins, annexin A2, which was identified by mass spectrometry analysis and had the highest score by Mascot data search, was further characterized and investigated for its role as an autoantigen. By confocal microscopic observation, SARS patient sera and anti-S2 antibodies were co-localized on A549 cells and both of them were co-localized with anti-annexin A2 antibodies. Anti-annexin A2 antibodies bound to purified S2 proteins, and anti-S2 bound to immunoprecipitated annexin A2 from A549 cell lysate in a dose-dependent manner. Furthermore, an increased surface expression and raft-structure distribution of annexin A2 was present in A549 cells after stimulation with SARS-induced cytokines interleukin-6 and interferon-gamma. Cytokine stimulation increased the binding capability of anti-S2 antibodies to human lung epithelial cells. Together, the upregulated expression of annexin A2 by SARS-associated cytokines and the cross-reactivity of anti-SARS-CoV S2 antibodies to annexin A2 may have implications in SARS disease pathogenesis.
DOI: 10.1016/j.molimm.2009.11.019
PubMed: 20015551
Affiliations:
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pubmed:20015551Le document en format XML
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<term>Autoantigens (immunology)</term>
<term>Cell Line, Tumor</term>
<term>Cross Reactions (immunology)</term>
<term>Epithelial Cells (immunology)</term>
<term>Epithelial Cells (pathology)</term>
<term>Epithelial Cells (virology)</term>
<term>Humans</term>
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<term>Severe Acute Respiratory Syndrome (immunology)</term>
<term>Severe Acute Respiratory Syndrome (pathology)</term>
<term>Severe Acute Respiratory Syndrome (virology)</term>
<term>Spike Glycoprotein, Coronavirus</term>
<term>Up-Regulation (drug effects)</term>
<term>Up-Regulation (immunology)</term>
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<term>Cellules épithéliales (anatomopathologie)</term>
<term>Cellules épithéliales (immunologie)</term>
<term>Cellules épithéliales (virologie)</term>
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<term>Humains</term>
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<term>Respiratory Mucosa</term>
<term>SARS Virus</term>
<term>Severe Acute Respiratory Syndrome</term>
<term>Up-Regulation</term>
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<front><div type="abstract" xml:lang="en">Severe acute respiratory syndrome-associated coronavirus (SARS-CoV) infection causes lung failure characterized by atypical pneumonia. We previously showed that antibodies against SARS-CoV spike domain 2 (S2) in the patient sera can cross-react with human lung epithelial cells; however, the autoantigen is not yet identified. In this study, we performed proteomic studies and identified several candidate autoantigens recognized by SARS patient sera in human lung type II epithelial cell A549. Among the candidate proteins, annexin A2, which was identified by mass spectrometry analysis and had the highest score by Mascot data search, was further characterized and investigated for its role as an autoantigen. By confocal microscopic observation, SARS patient sera and anti-S2 antibodies were co-localized on A549 cells and both of them were co-localized with anti-annexin A2 antibodies. Anti-annexin A2 antibodies bound to purified S2 proteins, and anti-S2 bound to immunoprecipitated annexin A2 from A549 cell lysate in a dose-dependent manner. Furthermore, an increased surface expression and raft-structure distribution of annexin A2 was present in A549 cells after stimulation with SARS-induced cytokines interleukin-6 and interferon-gamma. Cytokine stimulation increased the binding capability of anti-S2 antibodies to human lung epithelial cells. Together, the upregulated expression of annexin A2 by SARS-associated cytokines and the cross-reactivity of anti-SARS-CoV S2 antibodies to annexin A2 may have implications in SARS disease pathogenesis.</div>
</front>
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<DateCompleted><Year>2010</Year>
<Month>02</Month>
<Day>23</Day>
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<DateRevised><Year>2020</Year>
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<Title>Molecular immunology</Title>
<ISOAbbreviation>Mol. Immunol.</ISOAbbreviation>
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<ArticleTitle>Annexin A2 on lung epithelial cell surface is recognized by severe acute respiratory syndrome-associated coronavirus spike domain 2 antibodies.</ArticleTitle>
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<Abstract><AbstractText>Severe acute respiratory syndrome-associated coronavirus (SARS-CoV) infection causes lung failure characterized by atypical pneumonia. We previously showed that antibodies against SARS-CoV spike domain 2 (S2) in the patient sera can cross-react with human lung epithelial cells; however, the autoantigen is not yet identified. In this study, we performed proteomic studies and identified several candidate autoantigens recognized by SARS patient sera in human lung type II epithelial cell A549. Among the candidate proteins, annexin A2, which was identified by mass spectrometry analysis and had the highest score by Mascot data search, was further characterized and investigated for its role as an autoantigen. By confocal microscopic observation, SARS patient sera and anti-S2 antibodies were co-localized on A549 cells and both of them were co-localized with anti-annexin A2 antibodies. Anti-annexin A2 antibodies bound to purified S2 proteins, and anti-S2 bound to immunoprecipitated annexin A2 from A549 cell lysate in a dose-dependent manner. Furthermore, an increased surface expression and raft-structure distribution of annexin A2 was present in A549 cells after stimulation with SARS-induced cytokines interleukin-6 and interferon-gamma. Cytokine stimulation increased the binding capability of anti-S2 antibodies to human lung epithelial cells. Together, the upregulated expression of annexin A2 by SARS-associated cytokines and the cross-reactivity of anti-SARS-CoV S2 antibodies to annexin A2 may have implications in SARS disease pathogenesis.</AbstractText>
<CopyrightInformation>(c) 2009 Elsevier Ltd. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Fang</LastName>
<ForeName>Yi-Ting</ForeName>
<Initials>YT</Initials>
<AffiliationInfo><Affiliation>Institute of Basic Medical Sciences, National Cheng Kung University Medical College, Tainan, Taiwan.</Affiliation>
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<Author ValidYN="Y"><LastName>Lin</LastName>
<ForeName>Chiou-Feng</ForeName>
<Initials>CF</Initials>
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<Author ValidYN="Y"><LastName>Liao</LastName>
<ForeName>Pao-Chi</ForeName>
<Initials>PC</Initials>
</Author>
<Author ValidYN="Y"><LastName>Kuo</LastName>
<ForeName>Yu-Min</ForeName>
<Initials>YM</Initials>
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<Author ValidYN="Y"><LastName>Wang</LastName>
<ForeName>Shuying</ForeName>
<Initials>S</Initials>
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<Author ValidYN="Y"><LastName>Yeh</LastName>
<ForeName>Trai-Ming</ForeName>
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<Author ValidYN="Y"><LastName>Shieh</LastName>
<ForeName>Chi-Chang K</ForeName>
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<Author ValidYN="Y"><LastName>Su</LastName>
<ForeName>Ih-Jen</ForeName>
<Initials>IJ</Initials>
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<Author ValidYN="Y"><LastName>Lei</LastName>
<ForeName>Huan-Yao</ForeName>
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<Author ValidYN="Y"><LastName>Lin</LastName>
<ForeName>Yee-Shin</ForeName>
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<NameOfSubstance UI="C472822">ANXA2 protein, human</NameOfSubstance>
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<NameOfSubstance UI="D017306">Annexin A2</NameOfSubstance>
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<MeshHeading><DescriptorName UI="D004847" MajorTopicYN="N">Epithelial Cells</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
<QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName>
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<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
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