Induction and suppression of an autoimmune disease by oligomerized T cell epitopes: enhanced in vivo potency of encephalitogenic peptides.
Identifieur interne : 002599 ( PubMed/Corpus ); précédent : 002598; suivant : 002600Induction and suppression of an autoimmune disease by oligomerized T cell epitopes: enhanced in vivo potency of encephalitogenic peptides.
Auteurs : K. Falk ; O. Rötzschke ; L. Santambrogio ; M E Dorf ; C. Brosnan ; J L StromingerSource :
- The Journal of experimental medicine [ 0022-1007 ] ; 2000.
English descriptors
- KwdEn :
- Animals, Encephalomyelitis, Autoimmune, Experimental (immunology), Encephalomyelitis, Autoimmune, Experimental (pathology), Encephalomyelitis, Autoimmune, Experimental (prevention & control), Epitopes (immunology), Epitopes (pharmacology), Freund's Adjuvant, Immunosuppressive Agents (pharmacology), Lymphocyte Activation, Mice, Mice, Inbred AKR, Mice, Inbred BALB C, Mice, Inbred Strains, Myelin Basic Protein (genetics), Myelin Basic Protein (immunology), Myelin Basic Protein (pharmacology), Myelin Proteolipid Protein (genetics), Myelin Proteolipid Protein (immunology), Myelin Proteolipid Protein (pharmacology), Species Specificity, T-Lymphocytes (immunology), T-Lymphocytes (pathology), Time Factors.
- MESH :
- chemical , genetics : Myelin Basic Protein, Myelin Proteolipid Protein.
- chemical , immunology : Epitopes, Myelin Basic Protein, Myelin Proteolipid Protein.
- immunology : Encephalomyelitis, Autoimmune, Experimental, T-Lymphocytes.
- pathology : Encephalomyelitis, Autoimmune, Experimental, T-Lymphocytes.
- chemical , pharmacology : Epitopes, Immunosuppressive Agents, Myelin Basic Protein, Myelin Proteolipid Protein.
- prevention & control : Encephalomyelitis, Autoimmune, Experimental.
- Animals, Freund's Adjuvant, Lymphocyte Activation, Mice, Mice, Inbred AKR, Mice, Inbred BALB C, Mice, Inbred Strains, Species Specificity, Time Factors.
Abstract
T cell epitope peptides derived from proteolipid protein (PLP139-151) or myelin basic protein (MBP86-100) induce experimental autoimmune encephalomyelitis (EAE) in "susceptible" strains of mice (e.g., SJL/J). In this study, we show that the encephalitogenic effect of these epitopes when injected subcutaneously in complete Freund's adjuvant was significantly enhanced if administered to the animal in a multimerized form as a T cell epitope oligomer (i.e., as multiple repeats of the peptide epitope, such as 16-mers). Oligomer-treated SJL/J mice developed EAE faster and showed a more severe progression of the disease than animals treated with peptide alone. In addition, haplotype-matched B10.S mice, "resistant" to EAE induction by peptide, on injection of 16-mers developed a severe form of EAE. Even more striking, however, was the dramatic suppression of incidence and severity of the disease, seen after single intravenous injections of only 50 microg of the PLP139-151 16-mer, administered to SJL/J mice 7 d after the induction of the disease. Although relapse occurred at about day 45, an additional injection several days before that maintained the suppression. Importantly, the specific suppressive effect of oligomer treatment was also evident if EAE was induced with spinal cord homogenate instead of the single peptide antigen. By contrast, the PLP139-151 peptide accelerated rather than retarded the progression of disease.
DOI: 10.1084/jem.191.4.717
PubMed: 10684863
Links to Exploration step
pubmed:10684863Le document en format XML
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Brosnan</name></author><author><name sortKey="Strominger, J L" sort="Strominger, J L" uniqKey="Strominger J" first="J L" last="Strominger">J L Strominger</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2000">2000</date><idno type="RBID">pubmed:10684863</idno><idno type="pmid">10684863</idno><idno type="doi">10.1084/jem.191.4.717</idno><idno type="wicri:Area/PubMed/Corpus">002599</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002599</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Induction and suppression of an autoimmune disease by oligomerized T cell epitopes: enhanced in vivo potency of encephalitogenic peptides.</title><author><name sortKey="Falk, K" sort="Falk, K" uniqKey="Falk K" first="K" last="Falk">K. Falk</name><affiliation><nlm:affiliation>Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Rotzschke, O" sort="Rotzschke, O" uniqKey="Rotzschke O" first="O" last="Rötzschke">O. Rötzschke</name></author><author><name sortKey="Santambrogio, L" sort="Santambrogio, L" uniqKey="Santambrogio L" first="L" last="Santambrogio">L. Santambrogio</name></author><author><name sortKey="Dorf, M E" sort="Dorf, M E" uniqKey="Dorf M" first="M E" last="Dorf">M E Dorf</name></author><author><name sortKey="Brosnan, C" sort="Brosnan, C" uniqKey="Brosnan C" first="C" last="Brosnan">C. Brosnan</name></author><author><name sortKey="Strominger, J L" sort="Strominger, J L" uniqKey="Strominger J" first="J L" last="Strominger">J L Strominger</name></author></analytic><series><title level="j">The Journal of experimental medicine</title><idno type="ISSN">0022-1007</idno><imprint><date when="2000" type="published">2000</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Encephalomyelitis, Autoimmune, Experimental (immunology)</term><term>Encephalomyelitis, Autoimmune, Experimental (pathology)</term><term>Encephalomyelitis, Autoimmune, Experimental (prevention & control)</term><term>Epitopes (immunology)</term><term>Epitopes (pharmacology)</term><term>Freund's Adjuvant</term><term>Immunosuppressive Agents (pharmacology)</term><term>Lymphocyte Activation</term><term>Mice</term><term>Mice, Inbred AKR</term><term>Mice, Inbred BALB C</term><term>Mice, Inbred Strains</term><term>Myelin Basic Protein (genetics)</term><term>Myelin Basic Protein (immunology)</term><term>Myelin Basic Protein (pharmacology)</term><term>Myelin Proteolipid Protein (genetics)</term><term>Myelin Proteolipid Protein (immunology)</term><term>Myelin Proteolipid Protein (pharmacology)</term><term>Species Specificity</term><term>T-Lymphocytes (immunology)</term><term>T-Lymphocytes (pathology)</term><term>Time Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Myelin Basic Protein</term><term>Myelin Proteolipid Protein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Epitopes</term><term>Myelin Basic Protein</term><term>Myelin Proteolipid Protein</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Encephalomyelitis, Autoimmune, Experimental</term><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Encephalomyelitis, Autoimmune, Experimental</term><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Epitopes</term><term>Immunosuppressive Agents</term><term>Myelin Basic Protein</term><term>Myelin Proteolipid Protein</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Encephalomyelitis, Autoimmune, Experimental</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Freund's Adjuvant</term><term>Lymphocyte Activation</term><term>Mice</term><term>Mice, Inbred AKR</term><term>Mice, Inbred BALB C</term><term>Mice, Inbred Strains</term><term>Species Specificity</term><term>Time Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">T cell epitope peptides derived from proteolipid protein (PLP139-151) or myelin basic protein (MBP86-100) induce experimental autoimmune encephalomyelitis (EAE) in "susceptible" strains of mice (e.g., SJL/J). In this study, we show that the encephalitogenic effect of these epitopes when injected subcutaneously in complete Freund's adjuvant was significantly enhanced if administered to the animal in a multimerized form as a T cell epitope oligomer (i.e., as multiple repeats of the peptide epitope, such as 16-mers). Oligomer-treated SJL/J mice developed EAE faster and showed a more severe progression of the disease than animals treated with peptide alone. In addition, haplotype-matched B10.S mice, "resistant" to EAE induction by peptide, on injection of 16-mers developed a severe form of EAE. Even more striking, however, was the dramatic suppression of incidence and severity of the disease, seen after single intravenous injections of only 50 microg of the PLP139-151 16-mer, administered to SJL/J mice 7 d after the induction of the disease. Although relapse occurred at about day 45, an additional injection several days before that maintained the suppression. Importantly, the specific suppressive effect of oligomer treatment was also evident if EAE was induced with spinal cord homogenate instead of the single peptide antigen. By contrast, the PLP139-151 peptide accelerated rather than retarded the progression of disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">10684863</PMID><DateCompleted><Year>2000</Year><Month>04</Month><Day>19</Day></DateCompleted><DateRevised><Year>2019</Year><Month>05</Month><Day>08</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-1007</ISSN><JournalIssue CitedMedium="Print"><Volume>191</Volume><Issue>4</Issue><PubDate><Year>2000</Year><Month>Feb</Month><Day>21</Day></PubDate></JournalIssue><Title>The Journal of experimental medicine</Title><ISOAbbreviation>J. Exp. Med.</ISOAbbreviation></Journal><ArticleTitle>Induction and suppression of an autoimmune disease by oligomerized T cell epitopes: enhanced in vivo potency of encephalitogenic peptides.</ArticleTitle><Pagination><MedlinePgn>717-30</MedlinePgn></Pagination><Abstract><AbstractText>T cell epitope peptides derived from proteolipid protein (PLP139-151) or myelin basic protein (MBP86-100) induce experimental autoimmune encephalomyelitis (EAE) in "susceptible" strains of mice (e.g., SJL/J). In this study, we show that the encephalitogenic effect of these epitopes when injected subcutaneously in complete Freund's adjuvant was significantly enhanced if administered to the animal in a multimerized form as a T cell epitope oligomer (i.e., as multiple repeats of the peptide epitope, such as 16-mers). Oligomer-treated SJL/J mice developed EAE faster and showed a more severe progression of the disease than animals treated with peptide alone. In addition, haplotype-matched B10.S mice, "resistant" to EAE induction by peptide, on injection of 16-mers developed a severe form of EAE. Even more striking, however, was the dramatic suppression of incidence and severity of the disease, seen after single intravenous injections of only 50 microg of the PLP139-151 16-mer, administered to SJL/J mice 7 d after the induction of the disease. Although relapse occurred at about day 45, an additional injection several days before that maintained the suppression. Importantly, the specific suppressive effect of oligomer treatment was also evident if EAE was induced with spinal cord homogenate instead of the single peptide antigen. By contrast, the PLP139-151 peptide accelerated rather than retarded the progression of disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Falk</LastName><ForeName>K</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Molecular and Cellular Biology, Harvard University, Cambridge, Massachusetts 02138, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rötzschke</LastName><ForeName>O</ForeName><Initials>O</Initials></Author><Author ValidYN="Y"><LastName>Santambrogio</LastName><ForeName>L</ForeName><Initials>L</Initials></Author><Author ValidYN="Y"><LastName>Dorf</LastName><ForeName>M E</ForeName><Initials>ME</Initials></Author><Author ValidYN="Y"><LastName>Brosnan</LastName><ForeName>C</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Strominger</LastName><ForeName>J L</ForeName><Initials>JL</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>5R35-CA47554</GrantID><Acronym>CA</Acronym><Agency>NCI NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>N01-AI45198</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J Exp Med</MedlineTA><NlmUniqueID>2985109R</NlmUniqueID><ISSNLinking>0022-1007</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000939">Epitopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007166">Immunosuppressive Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004676">Myelin Basic Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018991">Myelin Proteolipid Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>9007-81-2</RegistryNumber><NameOfSubstance UI="D005620">Freund's Adjuvant</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004681" MajorTopicYN="N">Encephalomyelitis, Autoimmune, Experimental</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000517" MajorTopicYN="Y">prevention & control</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000939" MajorTopicYN="N">Epitopes</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000494" 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