pubmed-article:7836933 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:7836933 | lifeskim:mentions | umls-concept:C0030956 | lld:lifeskim |
pubmed-article:7836933 | lifeskim:mentions | umls-concept:C0023688 | lld:lifeskim |
pubmed-article:7836933 | lifeskim:mentions | umls-concept:C1155013 | lld:lifeskim |
pubmed-article:7836933 | lifeskim:mentions | umls-concept:C1709059 | lld:lifeskim |
pubmed-article:7836933 | lifeskim:mentions | umls-concept:C0205349 | lld:lifeskim |
pubmed-article:7836933 | lifeskim:mentions | umls-concept:C0205227 | lld:lifeskim |
pubmed-article:7836933 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:7836933 | pubmed:dateCreated | 1995-2-24 | lld:pubmed |
pubmed-article:7836933 | pubmed:abstractText | T cells potentially encounter numerous endogenous peptides during selection in the thymus and in the periphery. We examined the impact of an endogenous peptide on in vivo T cell development, using a TCR transgenic mouse model based on a hemoglobin-specific T cell clone. In these mice, the transgenic beta chains paired with endogenous alpha chains. This led to a serendipitous primary reactivity to Ser69 peptide, an altered peptide ligand of the Hbd (64-76) epitope of the parent clone. Two Ser69-reactive T cell populations were identified. A smaller population of the Ser69-reactive T cells responded both to Ser69 and Hbd (64-76). A majority reacted only to Ser69, and not to Hbd(64-76); in fact, Hbd(64-76) was a specific TCR antagonist for these Ser69-only-reactive T cells. Thus, in this unique experimental system, Ser69 became an agonist, and Hbd (64-76) was an antagonist. Endogenous presentation of the antagonist ligand in the thymus selectively eliminated the high-avidity cells, while sparing low-avidity cells in the Ser69-reactive T cell repertoire. These results highlight how specificity guides developing T cells through a network of ligands and indicate that the endogenous peptide pool has a profound effect on T cell development and repertoire. | lld:pubmed |
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pubmed-article:7836933 | pubmed:language | eng | lld:pubmed |
pubmed-article:7836933 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:7836933 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:7836933 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:7836933 | pubmed:month | Feb | lld:pubmed |
pubmed-article:7836933 | pubmed:issn | 0022-1007 | lld:pubmed |
pubmed-article:7836933 | pubmed:author | pubmed-author:AllenP MPM | lld:pubmed |
pubmed-article:7836933 | pubmed:author | pubmed-author:IkeA FAF | lld:pubmed |
pubmed-article:7836933 | pubmed:author | pubmed-author:EvavoldB DBD | lld:pubmed |
pubmed-article:7836933 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:7836933 | pubmed:day | 1 | lld:pubmed |
pubmed-article:7836933 | pubmed:volume | 181 | lld:pubmed |
pubmed-article:7836933 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:7836933 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:7836933 | pubmed:pagination | 805-10 | lld:pubmed |
pubmed-article:7836933 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:7836933 | pubmed:year | 1995 | lld:pubmed |
pubmed-article:7836933 | pubmed:articleTitle | Modulation of T cell development by an endogenous altered peptide ligand. | lld:pubmed |
pubmed-article:7836933 | pubmed:affiliation | Center for Immunology, Washington University School of Medicine, St. Louis, Missouri 63110. | lld:pubmed |
pubmed-article:7836933 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:7836933 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
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