pubmed-article:1728971 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1728971 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
pubmed-article:1728971 | lifeskim:mentions | umls-concept:C0042164 | lld:lifeskim |
pubmed-article:1728971 | lifeskim:mentions | umls-concept:C0001563 | lld:lifeskim |
pubmed-article:1728971 | lifeskim:mentions | umls-concept:C0030956 | lld:lifeskim |
pubmed-article:1728971 | lifeskim:mentions | umls-concept:C1708096 | lld:lifeskim |
pubmed-article:1728971 | lifeskim:mentions | umls-concept:C0443146 | lld:lifeskim |
pubmed-article:1728971 | lifeskim:mentions | umls-concept:C1419805 | lld:lifeskim |
pubmed-article:1728971 | lifeskim:mentions | umls-concept:C1517004 | lld:lifeskim |
pubmed-article:1728971 | lifeskim:mentions | umls-concept:C1334043 | lld:lifeskim |
pubmed-article:1728971 | lifeskim:mentions | umls-concept:C0301625 | lld:lifeskim |
pubmed-article:1728971 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:1728971 | pubmed:dateCreated | 1992-2-12 | lld:pubmed |
pubmed-article:1728971 | pubmed:abstractText | The oral administration of S-antigen fragment (a synthetic peptide designated as peptide M and known to be uveitopathogenic for rat, guinea pig, and monkey) to Lewis rats prior to challenge with an emulsion of peptide M and CFA resulted in either a total or partial suppression of experimental autoimmune uveitis (EAU), a T cell-mediated autoimmune disease studied as a model for human uveitis and experimental autoimmune pinealitis (EPA). Both the clinical and histopathologic manifestations of the disease were suppressed in a dose-dependent manner. Pinealitis associated with EAU was also suppressed by the oral administration of peptide M. Additionally, ingestion of a fragment of baker's yeast (Saccharomyces cerevisiae) histone H3, which has five consecutive amino acids identical to peptide M and which has been found to be uveitopathogenic in Lewis rats, induced tolerance to either peptide M or synthetic histone H3 peptide. In addition, the proliferative response to peptide M was inhibited in peptide M-fed rats. The suppression of EAU and in vitro lymphocyte proliferative responses to peptide M were observed to be antigen specific, since oral feeding of a control protein (BSA) exerted no suppressive effect. Furthermore, the T cells isolated from the spleen and lymph nodes of animals rendered tolerant by oral administration of peptide M can transfer protection against EAU adoptively. These results demonstrate that the oral administration of an autoantigen or its homologous peptide initiates an antigen-specific cellular mechanism which may ameliorate EAU. | lld:pubmed |
pubmed-article:1728971 | pubmed:language | eng | lld:pubmed |
pubmed-article:1728971 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1728971 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:1728971 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1728971 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1728971 | pubmed:month | Jan | lld:pubmed |
pubmed-article:1728971 | pubmed:issn | 0008-8749 | lld:pubmed |
pubmed-article:1728971 | pubmed:author | pubmed-author:SinghV KVK | lld:pubmed |
pubmed-article:1728971 | pubmed:author | pubmed-author:ShinoharaTT | lld:pubmed |
pubmed-article:1728971 | pubmed:author | pubmed-author:YamakiKK | lld:pubmed |
pubmed-article:1728971 | pubmed:author | pubmed-author:KalraH KHK | lld:pubmed |
pubmed-article:1728971 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1728971 | pubmed:volume | 139 | lld:pubmed |
pubmed-article:1728971 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1728971 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1728971 | pubmed:pagination | 81-90 | lld:pubmed |
pubmed-article:1728971 | pubmed:dateRevised | 2003-11-14 | lld:pubmed |
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pubmed-article:1728971 | pubmed:year | 1992 | lld:pubmed |
pubmed-article:1728971 | pubmed:articleTitle | Suppression of experimental autoimmune uveitis in rats by the oral administration of the uveitopathogenic S-antigen fragment or a cross-reactive homologous peptide. | lld:pubmed |
pubmed-article:1728971 | pubmed:affiliation | Molecular Biology Section, National Eye Institute, National Institutes of Health, Bethesda, Maryland 20892. | lld:pubmed |
pubmed-article:1728971 | pubmed:publicationType | Journal Article | lld:pubmed |
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