Epitope mapping of the Ro/SSA60KD autoantigen reveals disease‐specific antibody‐binding profiles
Identifieur interne : 000323 ( Istex/Curation ); précédent : 000322; suivant : 000324Epitope mapping of the Ro/SSA60KD autoantigen reveals disease‐specific antibody‐binding profiles
Auteurs : J. G. Routsias ; A. G. Tzioufas [Grèce] ; M. Sakarellos-Daitsiotis ; C. Sakarellos ; H. M. Moutsopoulos [Grèce]Source :
- European Journal of Clinical Investigation [ 0014-2972 ] ; 1996-06.
English descriptors
- Teeft :
- African swine fever virus, Amino, Amino acid, Amino acid sequence, Amino acid sequences, Amino acids, Antibody binding, Antigenic, Antigenic determinants, Arthritis rheum, Autoantibody, Autoantibody production, Autoantigen, Autoimmune, Autoimmune disease, Autoimmune diseases, Autoimmune sera, Blackwell science, Cambridge research biochemicals, Carboxy terminus, Cell types, Clinical investigation, Control peptides, Determinant, Discrete epitopes, Elisa, Epitope, Epitope mapping, Erythematosus, European journal, Hypothetical protein, Immunodominant regions, Inhibition experiments, Kalsvetekllkyleav, Kalsvetekllkyleav epitope, Kalsvetekllkyleav epitopes, Kalsvetekllkyleav peptide, Local identity, Lupus, Major antigenic determinants, Molecular forms, Molecular mimicry, National university, Ngwshkdllr, Ngwshkdllr epitope, Ngwshkdllr peptide, Normal sera, Other proteins, Patient sera, Peptide, Peptide synthesis, Peptides ngwshkdllr epitope, Positive sera, Preliminary criteria, Present study, Primary syndrome, Proc natl acad, Reactive peptide, Salmonella choleraesuis, Sequence similarities, Sequence similarity, Solid phase peptide synthesis, Substrate solution, Syndrome, Synthetic peptides, Systemic lupus erythematosus, Transcription factor, Useful information.
Abstract
Anti‐Ro60KD autoantibodies are commonly found in sera from patients with primary Sjögren's syndrome (SS) and systemic lupus erythematosus (SLE). In order to identify the epitopes of this autoantigen, 22 ‐mer, synthetic peptides overlapping by eight residues, and covering the entire sequence of the Ro60KD autoantigen were prepared. Three groups of sera were evaluated according to their autoantibody specificities. The first group consisted of monospecific anti Ro60KD sera from four patients with SLE and one with SS, the second one was composed of anti‐Ro60KD + anti‐La(SSB)‐positive sera from four patients with SS and the third group included three normal sera and one anti Ro52KD serum. It was found that sera from SLE patients interact with a common antigenic site spanning the sequence TKYKQRNGWSHKDLLRSHLKP (169–190) of the Ro60KD protein. On the other hand, sera from SS patients recognise the ELYKEKALSVETEKLLKYLEAV (211–232) region of this autoantigen. Determination of the minimal required peptide length for optimal antibody recognition showed that the defined epitopes can be shortened to the NGWSHKDLLR (175–184) and KALSVETEKLLKYLEAV (216–232) sequences respectively. Inhibition experiments using the Ro60KD antigen and soluble peptides corresponding to the 175–184 and 216–232 segments further confirmed the specific antibody binding. These results, although only a small number of sera were used, indicate that the Ro60KD autoantigen, which is not charac‐ terized by disease specificity, contains two discrete epitopes specifically recognized from SLE and SS patient sera. Finally, the sequence similarity of the NGWSHKDLLR (175–184) epitope with some of the HLA haplotypes, associated with anti‐Ro response, deserves to be noted.
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DOI: 10.1046/j.1365-2362.1996.186316.x
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J. G. Routsias<affiliation><mods:affiliation>The Laboratory of Organic Chemistry, University of Ioannina, 451 10 Ioannina, Greece, and</mods:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation><affiliation><mods:affiliation>The Laboratory of Organic Chemistry, University of Ioannina, 451 10 Ioannina, Greece, and</mods:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation><affiliation><mods:affiliation>The Laboratory of Organic Chemistry, University of Ioannina, 451 10 Ioannina, Greece, and</mods:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation>Le document en format XML
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G." last="Routsias">J. G. Routsias</name><affiliation><mods:affiliation>The Laboratory of Organic Chemistry, University of Ioannina, 451 10 Ioannina, Greece, and</mods:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation></author><author><name sortKey="Tzioufas, A G" sort="Tzioufas, A G" uniqKey="Tzioufas A" first="A. G." last="Tzioufas">A. G. Tzioufas</name><affiliation wicri:level="1"><mods:affiliation>Department of Pathophysiology, Medical School, National University of Athens, Greece</mods:affiliation><country xml:lang="fr">Grèce</country><wicri:regionArea>Department of Pathophysiology, Medical School, National University of Athens</wicri:regionArea></affiliation></author><author><name sortKey="Sakarellos Aitsiotis, M" sort="Sakarellos Aitsiotis, M" uniqKey="Sakarellos Aitsiotis M" first="M." last="Sakarellos-Daitsiotis">M. Sakarellos-Daitsiotis</name><affiliation><mods:affiliation>The Laboratory of Organic Chemistry, University of Ioannina, 451 10 Ioannina, Greece, and</mods:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation></author><author><name sortKey="Sakarellos, C" sort="Sakarellos, C" uniqKey="Sakarellos C" first="C." last="Sakarellos">C. Sakarellos</name><affiliation><mods:affiliation>The Laboratory of Organic Chemistry, University of Ioannina, 451 10 Ioannina, Greece, and</mods:affiliation><wicri:noCountry code="subField">and</wicri:noCountry></affiliation></author><author><name sortKey="Moutsopoulos, H M" sort="Moutsopoulos, H M" uniqKey="Moutsopoulos H" first="H. M." last="Moutsopoulos">H. M. Moutsopoulos</name><affiliation wicri:level="1"><mods:affiliation>Department of Pathophysiology, Medical School, National University of Athens, Greece</mods:affiliation><country xml:lang="fr">Grèce</country><wicri:regionArea>Department of Pathophysiology, Medical School, National University of Athens</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">European Journal of Clinical Investigation</title><title level="j" type="alt">EUROPEAN JOURNAL OF CLINICAL INVESTIGATION</title><idno type="ISSN">0014-2972</idno><idno type="eISSN">1365-2362</idno><imprint><biblScope unit="vol">26</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="514">514</biblScope><biblScope unit="page" to="521">521</biblScope><biblScope unit="page-count">8</biblScope><publisher>Blackwell Science Ltd</publisher><pubPlace>Oxford BSL</pubPlace><date type="published" when="1996-06">1996-06</date></imprint><idno type="ISSN">0014-2972</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0014-2972</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>African swine fever virus</term><term>Amino</term><term>Amino acid</term><term>Amino acid sequence</term><term>Amino acid sequences</term><term>Amino acids</term><term>Antibody binding</term><term>Antigenic</term><term>Antigenic determinants</term><term>Arthritis rheum</term><term>Autoantibody</term><term>Autoantibody production</term><term>Autoantigen</term><term>Autoimmune</term><term>Autoimmune disease</term><term>Autoimmune diseases</term><term>Autoimmune sera</term><term>Blackwell science</term><term>Cambridge research biochemicals</term><term>Carboxy terminus</term><term>Cell types</term><term>Clinical investigation</term><term>Control peptides</term><term>Determinant</term><term>Discrete epitopes</term><term>Elisa</term><term>Epitope</term><term>Epitope mapping</term><term>Erythematosus</term><term>European journal</term><term>Hypothetical protein</term><term>Immunodominant regions</term><term>Inhibition experiments</term><term>Kalsvetekllkyleav</term><term>Kalsvetekllkyleav epitope</term><term>Kalsvetekllkyleav epitopes</term><term>Kalsvetekllkyleav peptide</term><term>Local identity</term><term>Lupus</term><term>Major antigenic determinants</term><term>Molecular forms</term><term>Molecular mimicry</term><term>National university</term><term>Ngwshkdllr</term><term>Ngwshkdllr epitope</term><term>Ngwshkdllr peptide</term><term>Normal sera</term><term>Other proteins</term><term>Patient sera</term><term>Peptide</term><term>Peptide synthesis</term><term>Peptides ngwshkdllr epitope</term><term>Positive sera</term><term>Preliminary criteria</term><term>Present study</term><term>Primary syndrome</term><term>Proc natl acad</term><term>Reactive peptide</term><term>Salmonella choleraesuis</term><term>Sequence similarities</term><term>Sequence similarity</term><term>Solid phase peptide synthesis</term><term>Substrate solution</term><term>Syndrome</term><term>Synthetic peptides</term><term>Systemic lupus erythematosus</term><term>Transcription factor</term><term>Useful information</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Anti‐Ro60KD autoantibodies are commonly found in sera from patients with primary Sjögren's syndrome (SS) and systemic lupus erythematosus (SLE). In order to identify the epitopes of this autoantigen, 22 ‐mer, synthetic peptides overlapping by eight residues, and covering the entire sequence of the Ro60KD autoantigen were prepared. Three groups of sera were evaluated according to their autoantibody specificities. The first group consisted of monospecific anti Ro60KD sera from four patients with SLE and one with SS, the second one was composed of anti‐Ro60KD + anti‐La(SSB)‐positive sera from four patients with SS and the third group included three normal sera and one anti Ro52KD serum. It was found that sera from SLE patients interact with a common antigenic site spanning the sequence TKYKQRNGWSHKDLLRSHLKP (169–190) of the Ro60KD protein. On the other hand, sera from SS patients recognise the ELYKEKALSVETEKLLKYLEAV (211–232) region of this autoantigen. Determination of the minimal required peptide length for optimal antibody recognition showed that the defined epitopes can be shortened to the NGWSHKDLLR (175–184) and KALSVETEKLLKYLEAV (216–232) sequences respectively. Inhibition experiments using the Ro60KD antigen and soluble peptides corresponding to the 175–184 and 216–232 segments further confirmed the specific antibody binding. These results, although only a small number of sera were used, indicate that the Ro60KD autoantigen, which is not charac‐ terized by disease specificity, contains two discrete epitopes specifically recognized from SLE and SS patient sera. Finally, the sequence similarity of the NGWSHKDLLR (175–184) epitope with some of the HLA haplotypes, associated with anti‐Ro response, deserves to be noted.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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