| pubmed-article:1380066 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1380066 | lifeskim:mentions | umls-concept:C0014063 | lld:lifeskim |
| pubmed-article:1380066 | lifeskim:mentions | umls-concept:C0014072 | lld:lifeskim |
| pubmed-article:1380066 | lifeskim:mentions | umls-concept:C0030956 | lld:lifeskim |
| pubmed-article:1380066 | lifeskim:mentions | umls-concept:C1709915 | lld:lifeskim |
| pubmed-article:1380066 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:1380066 | lifeskim:mentions | umls-concept:C0302891 | lld:lifeskim |
| pubmed-article:1380066 | lifeskim:mentions | umls-concept:C0071505 | lld:lifeskim |
| pubmed-article:1380066 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:1380066 | pubmed:dateCreated | 1992-9-16 | lld:pubmed |
| pubmed-article:1380066 | pubmed:abstractText | The minimum structural requirements for peptide interactions with major histocompatibility complex (MHC) class II molecules and with T cell receptors (TCRs) were examined. In this report we show that substituting alanines at all but five amino acids in the myelin basic protein (MBP) peptide Ac1-11 does not alter its ability to bind A alpha uA beta u (MHC class II molecules), to stimulate specific T cells and, surprisingly, to induce experimental autoimmune encephalomyelitis (EAE) in (PL/J x SJL/J)F1 mice. Most other amino acid side chains in the Ac1-11 peptide are essentially irrelevant for T cell stimulation and for disease induction. Further analysis revealed that binding to A alpha uA beta u occurred with a peptide that consists mainly of alanines and only three of the original residues of Ac1-11. Moreover, when used as a coimmunogen with MBP Ac1-11, this peptide inhibited EAE. The finding that a specific in vivo response can be generated by a peptide containing only five native residues provides evidence that disease-inducing TCRs recognize only a very short sequence of the MHC-bound peptide. | lld:pubmed |
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| pubmed-article:1380066 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1380066 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1380066 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:1380066 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1380066 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:1380066 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:1380066 | pubmed:author | pubmed-author:McDevittH OHO | lld:pubmed |
| pubmed-article:1380066 | pubmed:author | pubmed-author:SteinmanLL | lld:pubmed |
| pubmed-article:1380066 | pubmed:author | pubmed-author:SmilekD EDE | lld:pubmed |
| pubmed-article:1380066 | pubmed:author | pubmed-author:GautamA MAM | lld:pubmed |
| pubmed-article:1380066 | pubmed:author | pubmed-author:PearsonC ICI | lld:pubmed |
| pubmed-article:1380066 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1380066 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:1380066 | pubmed:volume | 176 | lld:pubmed |
| pubmed-article:1380066 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1380066 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1380066 | pubmed:pagination | 605-9 | lld:pubmed |
| pubmed-article:1380066 | pubmed:dateRevised | 2010-9-7 | lld:pubmed |
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| pubmed-article:1380066 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1380066 | pubmed:articleTitle | A polyalanine peptide with only five native myelin basic protein residues induces autoimmune encephalomyelitis. | lld:pubmed |
| pubmed-article:1380066 | pubmed:affiliation | Department of Microbiology and Immunology, Stanford University School of Medicine, California 94305. | lld:pubmed |
| pubmed-article:1380066 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1380066 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1380066 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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