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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
1996-8-7
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pubmed:abstractText |
The specificity of the influenza nucleoprotein-induced T-cell proliferative response by mouse strains differing in either H-2- or non-H-2-linked background genes was compared by using a panel of synthetic peptides covering 90% of the nucleoprotein molecule. The results showed, as expected, that H-2 genes strongly influenced the major regions of the molecules recognized by T cells, as the response was focused on different peptides in mice of different H-2 haplotypes. However, some regions of the molecule (e.g. 260-283) were recognized by several different haplotypes, with overlapping but distinct minimal determinants. The lymph node proliferative response appeared to be predominantly restricted by the I-A molecule, as expression of I-E in mice did not result in any detectable recognition of additional epitopes. In the majority of cases the same T-cell epitopes were recognized by mouse strains sharing the same H-2 haplotype but differing in many background genes. Low responsiveness was however observed to p55-77 by DBA/2 and p127-141 by AKR mice to which other H-2d or H-2k strains were high responders. Low responsiveness is therefore unlikely to be a consequence of failure of these peptides to bind to the relevant major histocompatibility complex class II molecule. In addition antigen-presenting cells from the DBA/2 low responder strain was able to process and present whole influenza virus or nucleoprotein as well as antigen-presenting cells from the high responder BALB/c strain. It is therefore suggested that low responsiveness to the peptide p55-77 may be due to a 'hole in the T-cell repertoire', caused perhaps by expression of Mls-1a in the DBA/2 strain. This is supported by the observation that low responsiveness to this epitope appears to be dominant in F1 (low x high) mice.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-1530921,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-1656276,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-1690775,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-1698871,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-1713610,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-1715360,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-1719532,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-1846947,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-1846950,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-1972592,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-2056283,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-2138558,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-2435001,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-2456373,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-2477456,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-2478631,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-2953795,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-3126396,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-3126397,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-3263440,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-3456168,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-3518750,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-3876513,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-4998414,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-7689611,
http://linkedlifedata.com/resource/pubmed/commentcorrection/8666434-8436404
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Viral,
http://linkedlifedata.com/resource/pubmed/chemical/Epitopes,
http://linkedlifedata.com/resource/pubmed/chemical/H-2 Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class II,
http://linkedlifedata.com/resource/pubmed/chemical/NP protein, Influenza A virus,
http://linkedlifedata.com/resource/pubmed/chemical/Nucleoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/RNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Viral Core Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0019-2805
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
87
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
42-8
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:8666434-Animals,
pubmed-meshheading:8666434-Antigen-Presenting Cells,
pubmed-meshheading:8666434-Antigens, Viral,
pubmed-meshheading:8666434-CD4-Positive T-Lymphocytes,
pubmed-meshheading:8666434-Cell Culture Techniques,
pubmed-meshheading:8666434-Cell Division,
pubmed-meshheading:8666434-Epitopes,
pubmed-meshheading:8666434-Female,
pubmed-meshheading:8666434-Genes, MHC Class II,
pubmed-meshheading:8666434-H-2 Antigens,
pubmed-meshheading:8666434-Histocompatibility Antigens Class II,
pubmed-meshheading:8666434-Influenza A virus,
pubmed-meshheading:8666434-Mice,
pubmed-meshheading:8666434-Mice, Inbred Strains,
pubmed-meshheading:8666434-Mutation,
pubmed-meshheading:8666434-Nucleoproteins,
pubmed-meshheading:8666434-Peptide Fragments,
pubmed-meshheading:8666434-RNA-Binding Proteins,
pubmed-meshheading:8666434-Viral Core Proteins
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pubmed:year |
1996
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pubmed:articleTitle |
Both H-2- and non-H-2-linked genes influence influenza nucleoprotein epitope recognition by CD4+ T cells.
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pubmed:affiliation |
Molecular Immunology Group, Wellcome Research Laboratories, Beckenham, Kent, UK.
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pubmed:publicationType |
Journal Article
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