rdf:type |
|
lifeskim:mentions |
umls-concept:C0024518,
umls-concept:C0032659,
umls-concept:C0039194,
umls-concept:C0085358,
umls-concept:C0205402,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1549649,
umls-concept:C1706438,
umls-concept:C1880371,
umls-concept:C2348519,
umls-concept:C2349209,
umls-concept:C2698600
|
pubmed:issue |
4
|
pubmed:dateCreated |
2005-3-23
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pubmed:databankReference |
|
pubmed:abstractText |
Using both 'reverse genetics' and structural analysis, we have examined the in vivo relationship between antigenicity and T cell receptor (TCR) repertoire diversity. Influenza A virus infection of C57BL/6 mice induces profoundly different TCR repertoires specific for the nucleoprotein peptide of amino acids 366-374 (NP366) and the acid polymerase peptide of amino acids 224-233 (PA224) presented by H-2D(b). Here we show the H-2D(b)-NP366 complex with a 'featureless' structure selected a limited TCR repertoire characterized by 'public' TCR usage. In contrast, the prominent H-2D(b)-PA224 complex selected diverse, individually 'private' TCR repertoires. Substitution of the arginine at position 7 of PA224 with an alanine reduced the accessible side chains of the epitope. Infection with an engineered virus containing a mutation at the site encoding the exposed arginine at position 7 of PA224 selected a restricted TCR repertoire similar in diversity to that of the H-2D(b)-NP366-specific response. Thus, the lack of prominent features in an antigenic complex of peptide and major histocompatibility complex class I is associated with a diminished spectrum of TCR usage.
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pubmed:grant |
|
pubmed:commentsCorrections |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Apr
|
pubmed:issn |
1529-2908
|
pubmed:author |
pubmed-author:DohertyPeter CPC,
pubmed-author:DunstoneMichelle AMA,
pubmed-author:KedzierskaKatherineK,
pubmed-author:KomodromouHelenH,
pubmed-author:La GrutaNicole LNL,
pubmed-author:McCluskeyJamesJ,
pubmed-author:PurcellAnthony WAW,
pubmed-author:RossjohnJamieJ,
pubmed-author:TurnerStephen JSJ,
pubmed-author:WaldenHelenH,
pubmed-author:WebbAndrew IAI,
pubmed-author:WebbyRichardR,
pubmed-author:XieWiedongW
|
pubmed:issnType |
Print
|
pubmed:volume |
6
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
382-9
|
pubmed:dateRevised |
2007-11-14
|
pubmed:meshHeading |
pubmed-meshheading:15735650-Amino Acid Sequence,
pubmed-meshheading:15735650-Animals,
pubmed-meshheading:15735650-Antigenic Variation,
pubmed-meshheading:15735650-Antigens, Viral,
pubmed-meshheading:15735650-CD8-Positive T-Lymphocytes,
pubmed-meshheading:15735650-Crystallography, X-Ray,
pubmed-meshheading:15735650-Epitopes, T-Lymphocyte,
pubmed-meshheading:15735650-Histocompatibility Antigens,
pubmed-meshheading:15735650-Influenza A virus,
pubmed-meshheading:15735650-Mice,
pubmed-meshheading:15735650-Mice, Inbred C57BL,
pubmed-meshheading:15735650-Models, Molecular,
pubmed-meshheading:15735650-Molecular Sequence Data,
pubmed-meshheading:15735650-Orthomyxoviridae Infections,
pubmed-meshheading:15735650-Point Mutation,
pubmed-meshheading:15735650-Receptors, Antigen, T-Cell,
pubmed-meshheading:15735650-T-Lymphocytes, Cytotoxic
|
pubmed:year |
2005
|
pubmed:articleTitle |
Lack of prominent peptide-major histocompatibility complex features limits repertoire diversity in virus-specific CD8+ T cell populations.
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pubmed:affiliation |
Department of Microbiology and Immunology, The University of Melbourne, Parkville, Victoria 3010, Australia.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|