Predicting the effects of potentially therapeutic modified peptides on polyclonal T cell populations in a mouse model of multiple sclerosis.
Identifieur interne : 000B34 ( PubMed/Corpus ); précédent : 000B33; suivant : 000B35Predicting the effects of potentially therapeutic modified peptides on polyclonal T cell populations in a mouse model of multiple sclerosis.
Auteurs : Evan L. Sauer ; Elisabeth Trifilieff ; Judith M. GreerSource :
- Journal of neuroimmunology [ 1872-8421 ] ; 2017.
English descriptors
- KwdEn :
- Amino Acid Sequence, Animals, Antigen-Presenting Cells (drug effects), Antigen-Presenting Cells (immunology), Cell Proliferation (drug effects), Cytokines (genetics), Cytokines (metabolism), Disease Models, Animal, Encephalomyelitis, Autoimmune, Experimental (chemically induced), Encephalomyelitis, Autoimmune, Experimental (drug therapy), Encephalomyelitis, Autoimmune, Experimental (immunology), Encephalomyelitis, Autoimmune, Experimental (pathology), Epitopes (chemistry), Epitopes (immunology), Female, Flow Cytometry, Freund's Adjuvant (toxicity), Mice, Myelin Proteolipid Protein (chemistry), Myelin Proteolipid Protein (genetics), Myelin Proteolipid Protein (toxicity), Peptide Fragments (chemistry), Peptide Fragments (genetics), Peptide Fragments (immunology), Peptide Fragments (toxicity), RNA, Messenger, Receptors, Antigen, T-Cell, alpha-beta (genetics), Receptors, Antigen, T-Cell, alpha-beta (metabolism), T-Lymphocytes (drug effects), T-Lymphocytes (immunology), Th1 Cells (drug effects).
- MESH :
- chemical , chemistry : Epitopes, Myelin Proteolipid Protein, Peptide Fragments.
- chemical , genetics : Cytokines, Myelin Proteolipid Protein, Peptide Fragments, Receptors, Antigen, T-Cell, alpha-beta.
- chemically induced : Encephalomyelitis, Autoimmune, Experimental.
- drug effects : Antigen-Presenting Cells, Cell Proliferation, T-Lymphocytes, Th1 Cells.
- drug therapy : Encephalomyelitis, Autoimmune, Experimental.
- immunology : Antigen-Presenting Cells, Encephalomyelitis, Autoimmune, Experimental, Epitopes, Peptide Fragments, T-Lymphocytes.
- chemical , metabolism : Cytokines, Receptors, Antigen, T-Cell, alpha-beta.
- pathology : Encephalomyelitis, Autoimmune, Experimental.
- chemical , toxicity : Freund's Adjuvant, Myelin Proteolipid Protein, Peptide Fragments.
- Amino Acid Sequence, Animals, Disease Models, Animal, Female, Flow Cytometry, Mice, RNA, Messenger.
Abstract
Altered peptide ligands (APLs) have routinely been studied in clonal populations of Th cells that express a single T cell receptor (TCR), but results generated in this manner poorly predict the effects of APLs on polyclonal Th cells in vivo, contributing to the failure of phase II clinical trials of APLs in autoimmune diseases such as multiple sclerosis (MS). We have used a panel of APLs derived from an encephalitogenic epitope of myelin proteolipid protein to investigate the relationship between antigen cross-reactivity in a polyclonal environment, encephalitogenicity, and the capacity of an APL to provide protection against experimental autoimmune encephalomyelitis (EAE) in SJL mice. In general, polyclonal Th cell lines specific for encephalitogenic APLs cross-reacted with other encephalitogenic APLs, but not with non-encephalitogenic APLs, and vice versa. This, alongside analysis of TCR Vβ usage, suggested that encephalitogenic and non-encephalitogenic subgroups of APLs expand largely non-cross-reactive Th cell populations. As an exception to the rule, one non-encephalitogenic APL, L188, induced proliferation in polyclonal CD4(+) T cells specific for the native encephalitogen, with minimal induction of cytokine production. Co-immunization of L188 alongside the native encephalitogen slightly enhanced disease development. In contrast, another APL, A188, which induced IL-10 production without proliferation in CD4(+) T cells specific for the native encephalitogen, was able to protect against development of EAE in a dose-dependent fashion when co-immunized alongside the native encephalitogen. These results suggest that testing against polyclonal Th cell lines in vitro may be an effective strategy for distinguishing between potentially therapeutic and non-therapeutic APLs.
DOI: 10.1016/j.jneuroim.2017.03.011
PubMed: 28495132
Links to Exploration step
pubmed:28495132Le document en format XML
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Sauer</name><affiliation><nlm:affiliation>The University of Queensland, UQ Centre for Clinical Research, Brisbane, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Trifilieff, Elisabeth" sort="Trifilieff, Elisabeth" uniqKey="Trifilieff E" first="Elisabeth" last="Trifilieff">Elisabeth Trifilieff</name><affiliation><nlm:affiliation>Laboratoire d'Imagerie et de Neurosciences Cognitives (LINC), Université de Strasbourg/CNRS, France.</nlm:affiliation></affiliation></author><author><name sortKey="Greer, Judith M" sort="Greer, Judith M" uniqKey="Greer J" first="Judith M" last="Greer">Judith M. Greer</name><affiliation><nlm:affiliation>The University of Queensland, UQ Centre for Clinical Research, Brisbane, Australia. Electronic address: j.greer@uq.edu.au.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Journal of neuroimmunology</title><idno type="eISSN">1872-8421</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Amino Acid Sequence</term><term>Animals</term><term>Antigen-Presenting Cells (drug effects)</term><term>Antigen-Presenting Cells (immunology)</term><term>Cell Proliferation (drug effects)</term><term>Cytokines (genetics)</term><term>Cytokines (metabolism)</term><term>Disease Models, Animal</term><term>Encephalomyelitis, Autoimmune, Experimental (chemically induced)</term><term>Encephalomyelitis, Autoimmune, Experimental (drug therapy)</term><term>Encephalomyelitis, Autoimmune, Experimental (immunology)</term><term>Encephalomyelitis, Autoimmune, Experimental (pathology)</term><term>Epitopes (chemistry)</term><term>Epitopes (immunology)</term><term>Female</term><term>Flow Cytometry</term><term>Freund's Adjuvant (toxicity)</term><term>Mice</term><term>Myelin Proteolipid Protein (chemistry)</term><term>Myelin Proteolipid Protein (genetics)</term><term>Myelin Proteolipid Protein (toxicity)</term><term>Peptide Fragments (chemistry)</term><term>Peptide Fragments (genetics)</term><term>Peptide Fragments (immunology)</term><term>Peptide Fragments (toxicity)</term><term>RNA, Messenger</term><term>Receptors, Antigen, T-Cell, alpha-beta (genetics)</term><term>Receptors, Antigen, T-Cell, alpha-beta (metabolism)</term><term>T-Lymphocytes (drug effects)</term><term>T-Lymphocytes (immunology)</term><term>Th1 Cells (drug effects)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Epitopes</term><term>Myelin Proteolipid Protein</term><term>Peptide Fragments</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cytokines</term><term>Myelin Proteolipid Protein</term><term>Peptide Fragments</term><term>Receptors, Antigen, T-Cell, alpha-beta</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Encephalomyelitis, Autoimmune, Experimental</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Antigen-Presenting Cells</term><term>Cell Proliferation</term><term>T-Lymphocytes</term><term>Th1 Cells</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Encephalomyelitis, Autoimmune, Experimental</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Antigen-Presenting Cells</term><term>Encephalomyelitis, Autoimmune, Experimental</term><term>Epitopes</term><term>Peptide Fragments</term><term>T-Lymphocytes</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term><term>Receptors, Antigen, T-Cell, alpha-beta</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Encephalomyelitis, Autoimmune, Experimental</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Freund's Adjuvant</term><term>Myelin Proteolipid Protein</term><term>Peptide Fragments</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Amino Acid Sequence</term><term>Animals</term><term>Disease Models, Animal</term><term>Female</term><term>Flow Cytometry</term><term>Mice</term><term>RNA, Messenger</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Altered peptide ligands (APLs) have routinely been studied in clonal populations of Th cells that express a single T cell receptor (TCR), but results generated in this manner poorly predict the effects of APLs on polyclonal Th cells in vivo, contributing to the failure of phase II clinical trials of APLs in autoimmune diseases such as multiple sclerosis (MS). We have used a panel of APLs derived from an encephalitogenic epitope of myelin proteolipid protein to investigate the relationship between antigen cross-reactivity in a polyclonal environment, encephalitogenicity, and the capacity of an APL to provide protection against experimental autoimmune encephalomyelitis (EAE) in SJL mice. In general, polyclonal Th cell lines specific for encephalitogenic APLs cross-reacted with other encephalitogenic APLs, but not with non-encephalitogenic APLs, and vice versa. This, alongside analysis of TCR Vβ usage, suggested that encephalitogenic and non-encephalitogenic subgroups of APLs expand largely non-cross-reactive Th cell populations. As an exception to the rule, one non-encephalitogenic APL, L188, induced proliferation in polyclonal CD4(+) T cells specific for the native encephalitogen, with minimal induction of cytokine production. Co-immunization of L188 alongside the native encephalitogen slightly enhanced disease development. In contrast, another APL, A188, which induced IL-10 production without proliferation in CD4(+) T cells specific for the native encephalitogen, was able to protect against development of EAE in a dose-dependent fashion when co-immunized alongside the native encephalitogen. These results suggest that testing against polyclonal Th cell lines in vitro may be an effective strategy for distinguishing between potentially therapeutic and non-therapeutic APLs.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28495132</PMID><DateCreated><Year>2017</Year><Month>05</Month><Day>12</Day></DateCreated><DateCompleted><Year>2017</Year><Month>08</Month><Day>17</Day></DateCompleted><DateRevised><Year>2017</Year><Month>08</Month><Day>17</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-8421</ISSN><JournalIssue CitedMedium="Internet"><Volume>307</Volume><PubDate><Year>2017</Year><Month>Jun</Month><Day>15</Day></PubDate></JournalIssue><Title>Journal of neuroimmunology</Title><ISOAbbreviation>J. Neuroimmunol.</ISOAbbreviation></Journal><ArticleTitle>Predicting the effects of potentially therapeutic modified peptides on polyclonal T cell populations in a mouse model of multiple sclerosis.</ArticleTitle><Pagination><MedlinePgn>18-26</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0165-5728(16)30356-3</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jneuroim.2017.03.011</ELocationID><Abstract><AbstractText>Altered peptide ligands (APLs) have routinely been studied in clonal populations of Th cells that express a single T cell receptor (TCR), but results generated in this manner poorly predict the effects of APLs on polyclonal Th cells in vivo, contributing to the failure of phase II clinical trials of APLs in autoimmune diseases such as multiple sclerosis (MS). We have used a panel of APLs derived from an encephalitogenic epitope of myelin proteolipid protein to investigate the relationship between antigen cross-reactivity in a polyclonal environment, encephalitogenicity, and the capacity of an APL to provide protection against experimental autoimmune encephalomyelitis (EAE) in SJL mice. In general, polyclonal Th cell lines specific for encephalitogenic APLs cross-reacted with other encephalitogenic APLs, but not with non-encephalitogenic APLs, and vice versa. This, alongside analysis of TCR Vβ usage, suggested that encephalitogenic and non-encephalitogenic subgroups of APLs expand largely non-cross-reactive Th cell populations. As an exception to the rule, one non-encephalitogenic APL, L188, induced proliferation in polyclonal CD4(+) T cells specific for the native encephalitogen, with minimal induction of cytokine production. Co-immunization of L188 alongside the native encephalitogen slightly enhanced disease development. In contrast, another APL, A188, which induced IL-10 production without proliferation in CD4(+) T cells specific for the native encephalitogen, was able to protect against development of EAE in a dose-dependent fashion when co-immunized alongside the native encephalitogen. These results suggest that testing against polyclonal Th cell lines in vitro may be an effective strategy for distinguishing between potentially therapeutic and non-therapeutic APLs.</AbstractText><CopyrightInformation>Copyright © 2017 Elsevier B.V. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Sauer</LastName><ForeName>Evan L</ForeName><Initials>EL</Initials><AffiliationInfo><Affiliation>The University of Queensland, UQ Centre for Clinical Research, Brisbane, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Trifilieff</LastName><ForeName>Elisabeth</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Laboratoire d'Imagerie et de Neurosciences Cognitives (LINC), Université de Strasbourg/CNRS, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Greer</LastName><ForeName>Judith M</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>The University of Queensland, UQ Centre for Clinical Research, Brisbane, Australia. Electronic address: j.greer@uq.edu.au.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>03</Month><Day>21</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>J Neuroimmunol</MedlineTA><NlmUniqueID>8109498</NlmUniqueID><ISSNLinking>0165-5728</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016207">Cytokines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000939">Epitopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D018991">Myelin Proteolipid Protein</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010446">Peptide 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