Please use this identifier to cite or link to this item:
https://doi.org/10.1371/journal.pone.0064888
DC Field | Value | |
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dc.title | Active Suppression Induced by Repetitive Self-Epitopes Protects against EAE Development | |
dc.contributor.author | Puentes F. | |
dc.contributor.author | Dickhaut K. | |
dc.contributor.author | Hofstätter M. | |
dc.contributor.author | Falk K. | |
dc.contributor.author | Röetzschke O. | |
dc.date.accessioned | 2020-04-08T04:46:48Z | |
dc.date.available | 2020-04-08T04:46:48Z | |
dc.date.issued | 2013 | |
dc.identifier.citation | Puentes F., Dickhaut K., Hofstätter M., Falk K., Röetzschke O. (2013). Active Suppression Induced by Repetitive Self-Epitopes Protects against EAE Development. PLoS ONE 8 (5) : e64888. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0064888 | |
dc.identifier.issn | 19326203 | |
dc.identifier.uri | https://scholarbank.nus.edu.sg/handle/10635/166574 | |
dc.description.abstract | Background:Autoimmune diseases result from a breakdown in self-tolerance to autoantigens. Self-tolerance is induced and sustained by central and peripheral mechanisms intended to deviate harmful immune responses and to maintain homeostasis, where regulatory T cells play a crucial role. The use of self-antigens in the study and treatment of a range of autoimmune diseases has been widely described; however, the mechanisms underlying the induced protection by these means are unclear. This study shows that protection of experimental autoimmune disease induced by T cell self-epitopes in a multimerized form (oligomers) is mediated by the induction of active suppression.Principal Findings:The experimental autoimmune encephalomyelitis (EAE) animal model for multiple sclerosis was used to study the mechanisms of protection induced by the treatment of oligomerized T cell epitope of myelin proteolipid protein (PLP139-151). Disease protection attained by the administration of oligomers was shown to be antigen specific and effective in both prevention and treatment of ongoing EAE. Oligomer mediated tolerance was actively transferred by cells from treated mice into adoptive hosts. The induction of active suppression was correlated with the recruitment of cells in the periphery associated with increased production of IL-10 and reduction of the pro-inflammatory cytokine TNF-?. The role of suppressive cytokines was demonstrated by the reversion of oligomer-induced protection after in vivo blocking of either IL-10 or TGF-? cytokines.Conclusions:This study strongly supports an immunosuppressive role of repeat auto-antigens to control the development of EAE with potential applications in vaccination and antigen specific treatment of autoimmune diseases. © 2013 Puentes et al. | |
dc.publisher | Public Library of Science | |
dc.source | Unpaywall 20200320 | |
dc.subject | epitope | |
dc.subject | Freund adjuvant | |
dc.subject | immunosuppressive agent | |
dc.subject | myelin proteolipid protein[139-151] | |
dc.subject | oligomer | |
dc.subject | serylvalylserylserylphenylalanylglutamylarginylphenylalanylglutamylisoleucylphenylalalnylprolyllysine | |
dc.subject | synthetic peptide | |
dc.subject | T lymphocyte antigen | |
dc.subject | transforming growth factor beta | |
dc.subject | tumor necrosis factor alpha | |
dc.subject | unclassified drug | |
dc.subject | adoptive transfer | |
dc.subject | allergic encephalomyelitis | |
dc.subject | animal cell | |
dc.subject | animal experiment | |
dc.subject | animal model | |
dc.subject | animal tissue | |
dc.subject | antigen specificity | |
dc.subject | article | |
dc.subject | controlled study | |
dc.subject | cytokine production | |
dc.subject | disease control | |
dc.subject | ex vivo study | |
dc.subject | female | |
dc.subject | immunological tolerance | |
dc.subject | immunoprophylaxis | |
dc.subject | immunosuppressive treatment | |
dc.subject | in vivo study | |
dc.subject | lymphocyte proliferation | |
dc.subject | mouse | |
dc.subject | multiple sclerosis | |
dc.subject | nonhuman | |
dc.subject | oligomerization | |
dc.subject | treatment outcome | |
dc.subject | Adoptive Transfer | |
dc.subject | Animals | |
dc.subject | Autoantigens | |
dc.subject | Cell Proliferation | |
dc.subject | Cytokines | |
dc.subject | Encephalomyelitis, Autoimmune, Experimental | |
dc.subject | Epitopes, T-Lymphocyte | |
dc.subject | Female | |
dc.subject | Immunosuppression | |
dc.subject | Mice | |
dc.subject | Myelin Proteolipid Protein | |
dc.subject | Peptide Fragments | |
dc.subject | Protein Multimerization | |
dc.subject | Protein Structure, Quaternary | |
dc.subject | T-Lymphocytes | |
dc.subject | Animalia | |
dc.subject | Mus | |
dc.type | Article | |
dc.contributor.department | MICROBIOLOGY AND IMMUNOLOGY | |
dc.description.doi | 10.1371/journal.pone.0064888 | |
dc.description.sourcetitle | PLoS ONE | |
dc.description.volume | 8 | |
dc.description.issue | 5 | |
dc.description.page | e64888 | |
Appears in Collections: | Staff Publications Elements |
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