Random phage-epitope library based identification of a peptide antagonist of Mac-1 β2 integrin ligand binding.
Identifieur interne : 000653 ( Main/Exploration ); précédent : 000652; suivant : 000654Random phage-epitope library based identification of a peptide antagonist of Mac-1 β2 integrin ligand binding.
Auteurs : Mehdi Houimel [Tunisie] ; Luca MazzucchelliSource :
- Matrix biology : journal of the International Society for Matrix Biology [ 1569-1802 ] ; 2012.
Descripteurs français
- KwdFr :
- Adhérence cellulaire (MeSH), Anti-inflammatoires (composition chimique), Anti-inflammatoires (pharmacologie), Anticorps monoclonaux (MeSH), Antigène macrophage 1 (composition chimique), Antigène macrophage 1 (génétique), Antigène macrophage 1 (métabolisme), Antigènes CD11b (génétique), Antigènes CD11b (métabolisme), Antigènes CD18 (composition chimique), Antigènes CD18 (génétique), Antigènes CD18 (métabolisme), Banque de peptides (MeSH), Cartographie épitopique (méthodes), Complément C3b (métabolisme), Fibrinogène (métabolisme), Granulocytes neutrophiles (métabolisme), Humains (MeSH), Liaison aux protéines (MeSH), Peptides (antagonistes et inhibiteurs), Peptides (composition chimique), Peptides (métabolisme), Peptides cycliques (antagonistes et inhibiteurs), Récepteur du fibrinogène (antagonistes et inhibiteurs), Sites de fixation (MeSH).
- MESH :
- antagonistes et inhibiteurs : Peptides, Peptides cycliques, Récepteur du fibrinogène.
- composition chimique : Anti-inflammatoires, Antigène macrophage 1, Antigènes CD18, Peptides.
- génétique : Antigène macrophage 1, Antigènes CD11b, Antigènes CD18.
- métabolisme : Antigène macrophage 1, Antigènes CD11b, Antigènes CD18, Complément C3b, Fibrinogène, Granulocytes neutrophiles, Peptides.
- méthodes : Cartographie épitopique.
- pharmacologie : Anti-inflammatoires.
- Adhérence cellulaire, Anticorps monoclonaux, Banque de peptides, Humains, Liaison aux protéines, Sites de fixation.
English descriptors
- KwdEn :
- Anti-Inflammatory Agents (chemistry), Anti-Inflammatory Agents (pharmacology), Antibodies, Monoclonal (MeSH), Binding Sites (MeSH), CD11b Antigen (genetics), CD11b Antigen (metabolism), CD18 Antigens (chemistry), CD18 Antigens (genetics), CD18 Antigens (metabolism), Cell Adhesion (MeSH), Complement C3b (metabolism), Epitope Mapping (methods), Fibrinogen (metabolism), Humans (MeSH), Macrophage-1 Antigen (chemistry), Macrophage-1 Antigen (genetics), Macrophage-1 Antigen (metabolism), Neutrophils (metabolism), Peptide Library (MeSH), Peptides (antagonists & inhibitors), Peptides (chemistry), Peptides (metabolism), Peptides, Cyclic (antagonists & inhibitors), Protein Binding (MeSH), Receptors, Fibrinogen (antagonists & inhibitors).
- MESH :
- chemical , antagonists & inhibitors : Peptides, Peptides, Cyclic, Receptors, Fibrinogen.
- chemical , chemistry : Anti-Inflammatory Agents, CD18 Antigens, Macrophage-1 Antigen, Peptides.
- chemical , genetics : CD11b Antigen, CD18 Antigens, Macrophage-1 Antigen.
- chemical , metabolism : CD11b Antigen, CD18 Antigens, Complement C3b, Fibrinogen, Macrophage-1 Antigen, Peptides.
- chemical , pharmacology : Anti-Inflammatory Agents.
- chemical : Antibodies, Monoclonal, Peptide Library.
- metabolism : Neutrophils.
- methods : Epitope Mapping.
- Binding Sites, Cell Adhesion, Humans, Protein Binding.
Abstract
The leukocyte β2 integrin Mac-1 (CD11b/CD18) plays a pivotal role in inflammation and host defense. To develop peptide antagonists selectively inhibiting the function of Mac-1, we used a random constrained 6-mer (cys-6aa-cys) peptide library to map the structural features of CD11b, by determining the epitope of neutralizing monoclonal antibody mAb 44a (anti-CD11b). We have used a stringent phage display strategy, which resulted in the identification of one disulfide C-RLKEKH-C constrained peptide by direct biopanning of library on decreasing amounts of purified mAb 44a. The selected peptide mimics a discontinuous epitope, a peculiar shape on the CD11b-I-domain surface. Competitive ELISA experiments with different Mac-1 ligands showed that C-RLKEKH-C is able to bind to fibrinogen, iC3b, and C1q. Furthermore, the monomeric circular peptide C-RLKEKH-C, was effective in blocking the interaction between (125)I-fibrinogen and Mac-1 (IC(50)=3.35±0.1×10(-6)M), and inhibited the adhesion of human neutrophils to fibrinogen and iC3b. These data provide information about the relative location of amino acids on the I-domain surface using mAb 44a imprint of the CD11b protein. The derived mimotope may help in the design of future anti-inflammatory therapeutic agents that can act as specific therapeutic agents targeting PMNs mediated inflammation.
DOI: 10.1016/j.matbio.2011.10.003
PubMed: 22100634
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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mehdi.houimel@pasteur.rns.tn</nlm:affiliation><country xml:lang="fr">Tunisie</country><wicri:regionArea>Laboratoire d'Immunopathologie Vaccinologie et Génétique Moléculaire, Institut Pasteur de Tunis</wicri:regionArea><wicri:noRegion>Institut Pasteur de Tunis</wicri:noRegion></affiliation></author><author><name sortKey="Mazzucchelli, Luca" sort="Mazzucchelli, Luca" uniqKey="Mazzucchelli L" first="Luca" last="Mazzucchelli">Luca Mazzucchelli</name></author></analytic><series><title level="j">Matrix biology : journal of the International Society for Matrix Biology</title><idno type="eISSN">1569-1802</idno><imprint><date when="2012" type="published">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Anti-Inflammatory Agents (chemistry)</term><term>Anti-Inflammatory Agents (pharmacology)</term><term>Antibodies, Monoclonal (MeSH)</term><term>Binding Sites (MeSH)</term><term>CD11b Antigen (genetics)</term><term>CD11b Antigen (metabolism)</term><term>CD18 Antigens (chemistry)</term><term>CD18 Antigens (genetics)</term><term>CD18 Antigens (metabolism)</term><term>Cell Adhesion (MeSH)</term><term>Complement C3b (metabolism)</term><term>Epitope Mapping (methods)</term><term>Fibrinogen (metabolism)</term><term>Humans (MeSH)</term><term>Macrophage-1 Antigen (chemistry)</term><term>Macrophage-1 Antigen (genetics)</term><term>Macrophage-1 Antigen (metabolism)</term><term>Neutrophils (metabolism)</term><term>Peptide Library (MeSH)</term><term>Peptides (antagonists & inhibitors)</term><term>Peptides (chemistry)</term><term>Peptides (metabolism)</term><term>Peptides, Cyclic (antagonists & inhibitors)</term><term>Protein Binding (MeSH)</term><term>Receptors, Fibrinogen (antagonists & inhibitors)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adhérence cellulaire (MeSH)</term><term>Anti-inflammatoires (composition chimique)</term><term>Anti-inflammatoires 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(MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Peptides</term><term>Peptides, Cyclic</term><term>Receptors, Fibrinogen</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Anti-Inflammatory Agents</term><term>CD18 Antigens</term><term>Macrophage-1 Antigen</term><term>Peptides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>CD11b Antigen</term><term>CD18 Antigens</term><term>Macrophage-1 Antigen</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>CD11b Antigen</term><term>CD18 Antigens</term><term>Complement C3b</term><term>Fibrinogen</term><term>Macrophage-1 Antigen</term><term>Peptides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Anti-Inflammatory Agents</term></keywords><keywords scheme="MESH" type="chemical" 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C3b</term><term>Fibrinogène</term><term>Granulocytes neutrophiles</term><term>Peptides</term></keywords><keywords scheme="MESH" qualifier="méthodes" xml:lang="fr"><term>Cartographie épitopique</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Anti-inflammatoires</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Binding Sites</term><term>Cell Adhesion</term><term>Humans</term><term>Protein Binding</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adhérence cellulaire</term><term>Anticorps monoclonaux</term><term>Banque de peptides</term><term>Humains</term><term>Liaison aux protéines</term><term>Sites de fixation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The leukocyte β2 integrin Mac-1 (CD11b/CD18) plays a pivotal role in inflammation and host defense. To develop peptide antagonists selectively inhibiting the function of Mac-1, we used a random constrained 6-mer (cys-6aa-cys) peptide library to map the structural features of CD11b, by determining the epitope of neutralizing monoclonal antibody mAb 44a (anti-CD11b). We have used a stringent phage display strategy, which resulted in the identification of one disulfide C-RLKEKH-C constrained peptide by direct biopanning of library on decreasing amounts of purified mAb 44a. The selected peptide mimics a discontinuous epitope, a peculiar shape on the CD11b-I-domain surface. Competitive ELISA experiments with different Mac-1 ligands showed that C-RLKEKH-C is able to bind to fibrinogen, iC3b, and C1q. Furthermore, the monomeric circular peptide C-RLKEKH-C, was effective in blocking the interaction between (125)I-fibrinogen and Mac-1 (IC(50)=3.35±0.1×10(-6)M), and inhibited the adhesion of human neutrophils to fibrinogen and iC3b. These data provide information about the relative location of amino acids on the I-domain surface using mAb 44a imprint of the CD11b protein. The derived mimotope may help in the design of future anti-inflammatory therapeutic agents that can act as specific therapeutic agents targeting PMNs mediated inflammation.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">22100634</PMID><DateCompleted><Year>2012</Year><Month>05</Month><Day>03</Day></DateCompleted><DateRevised><Year>2017</Year><Month>11</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1569-1802</ISSN><JournalIssue CitedMedium="Internet"><Volume>31</Volume><Issue>1</Issue><PubDate><Year>2012</Year><Month>Jan</Month></PubDate></JournalIssue><Title>Matrix biology : journal of the International Society for Matrix Biology</Title><ISOAbbreviation>Matrix Biol</ISOAbbreviation></Journal><ArticleTitle>Random phage-epitope library based identification of a peptide antagonist of Mac-1 β2 integrin ligand binding.</ArticleTitle><Pagination><MedlinePgn>66-77</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.matbio.2011.10.003</ELocationID><Abstract><AbstractText>The leukocyte β2 integrin Mac-1 (CD11b/CD18) plays a pivotal role in inflammation and host defense. To develop peptide antagonists selectively inhibiting the function of Mac-1, we used a random constrained 6-mer (cys-6aa-cys) peptide library to map the structural features of CD11b, by determining the epitope of neutralizing monoclonal antibody mAb 44a (anti-CD11b). We have used a stringent phage display strategy, which resulted in the identification of one disulfide C-RLKEKH-C constrained peptide by direct biopanning of library on decreasing amounts of purified mAb 44a. The selected peptide mimics a discontinuous epitope, a peculiar shape on the CD11b-I-domain surface. Competitive ELISA experiments with different Mac-1 ligands showed that C-RLKEKH-C is able to bind to fibrinogen, iC3b, and C1q. Furthermore, the monomeric circular peptide C-RLKEKH-C, was effective in blocking the interaction between (125)I-fibrinogen and Mac-1 (IC(50)=3.35±0.1×10(-6)M), and inhibited the adhesion of human neutrophils to fibrinogen and iC3b. These data provide information about the relative location of amino acids on the I-domain surface using mAb 44a imprint of the CD11b protein. The derived mimotope may help in the design of future anti-inflammatory therapeutic agents that can act as specific therapeutic agents targeting PMNs mediated inflammation.</AbstractText><CopyrightInformation>Copyright © 2011 International Society of Matrix Biology. Published by Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Houimel</LastName><ForeName>Mehdi</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Laboratoire d'Immunopathologie Vaccinologie et Génétique Moléculaire, Institut Pasteur de Tunis, Tunisia. mehdi.houimel@pasteur.rns.tn</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mazzucchelli</LastName><ForeName>Luca</ForeName><Initials>L</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2011</Year><Month>11</Month><Day>11</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Matrix Biol</MedlineTA><NlmUniqueID>9432592</NlmUniqueID><ISSNLinking>0945-053X</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000893">Anti-Inflammatory Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000911">Antibodies, Monoclonal</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D039481">CD11b Antigen</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018821">CD18 Antigens</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016177">Macrophage-1 Antigen</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019151">Peptide Library</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010455">Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010456">Peptides, Cyclic</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D039341">Receptors, Fibrinogen</NameOfSubstance></Chemical><Chemical><RegistryNumber>80295-43-8</RegistryNumber><NameOfSubstance UI="D003179">Complement C3b</NameOfSubstance></Chemical><Chemical><RegistryNumber>9001-32-5</RegistryNumber><NameOfSubstance UI="D005340">Fibrinogen</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000893" MajorTopicYN="N">Anti-Inflammatory Agents</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000911" MajorTopicYN="N">Antibodies, Monoclonal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001665" MajorTopicYN="N">Binding Sites</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D039481" MajorTopicYN="N">CD11b Antigen</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018821" MajorTopicYN="N">CD18 Antigens</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002448" MajorTopicYN="N">Cell Adhesion</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003179" MajorTopicYN="N">Complement C3b</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018604" MajorTopicYN="N">Epitope Mapping</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="Y">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005340" MajorTopicYN="N">Fibrinogen</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D016177" MajorTopicYN="N">Macrophage-1 Antigen</DescriptorName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009504" MajorTopicYN="N">Neutrophils</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019151" MajorTopicYN="N">Peptide Library</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010455" MajorTopicYN="N">Peptides</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010456" MajorTopicYN="N">Peptides, Cyclic</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011485" MajorTopicYN="N">Protein Binding</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D039341" MajorTopicYN="N">Receptors, Fibrinogen</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2011</Year><Month>06</Month><Day>02</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2011</Year><Month>10</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2011</Year><Month>10</Month><Day>25</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>11</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>11</Month><Day>22</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2012</Year><Month>5</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">22100634</ArticleId><ArticleId IdType="pii">S0945-053X(11)00105-3</ArticleId><ArticleId IdType="doi">10.1016/j.matbio.2011.10.003</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Tunisie</li></country></list><tree><noCountry><name sortKey="Mazzucchelli, Luca" sort="Mazzucchelli, Luca" uniqKey="Mazzucchelli L" first="Luca" last="Mazzucchelli">Luca Mazzucchelli</name></noCountry><country name="Tunisie"><noRegion><name sortKey="Houimel, Mehdi" sort="Houimel, Mehdi" uniqKey="Houimel M" first="Mehdi" last="Houimel">Mehdi Houimel</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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