rdf:type |
|
lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0017349,
umls-concept:C0039194,
umls-concept:C0040113,
umls-concept:C0085358,
umls-concept:C0185117,
umls-concept:C0205359,
umls-concept:C0205734,
umls-concept:C0567416,
umls-concept:C1274040,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1442161,
umls-concept:C1519606,
umls-concept:C1706438,
umls-concept:C2698600,
umls-concept:C2911684
|
pubmed:issue |
2
|
pubmed:dateCreated |
2004-1-6
|
pubmed:abstractText |
H-2(d) mice expressing both the influenza virus hemagglutinin (HA) as a transgene-encoded protein on pancreatic islet beta cells (InsHA), as well as the Clone 4 TCR specific for the dominant H-2K(d)-restricted HA epitope, can be protected from the development of spontaneous autoimmune diabetes by expression of the H-2(b) haplotype. Protection occurs due to the deletion of K(d)HA-specific CD8+ T cells. This was unexpected as neither the presence of the InsHA transgene nor H-2(b), individually, resulted in thymic deletion. Further analyses revealed that thymic deletion required both a hybrid MHC class II molecule, Ebeta(b) Ealpha(d), and the K(d) molecule presenting the HA epitope, which together synergize to effect deletion of CD4+CD8+ thymocytes. This surprising example of protection from autoimmunity that maps to a class II MHC molecule, yet effects an alteration in the CD8+ T cell repertoire, suggests that selective events in the thymus represent the integrated strength of signal delivered to each cell through recognition of a variety of different MHC-peptide ligands.
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pubmed:grant |
|
pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD4,
http://linkedlifedata.com/resource/pubmed/chemical/H-2 Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/H-2K(K) antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Hemagglutinin Glycoproteins...,
http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class II,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell,
http://linkedlifedata.com/resource/pubmed/chemical/histocompatibility antigen H-2D(b)
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
|
pubmed:issn |
0022-1767
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pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
15
|
pubmed:volume |
172
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
1000-8
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:14707073-Animals,
pubmed-meshheading:14707073-Animals, Newborn,
pubmed-meshheading:14707073-Antigens, CD4,
pubmed-meshheading:14707073-CD8-Positive T-Lymphocytes,
pubmed-meshheading:14707073-Cell Differentiation,
pubmed-meshheading:14707073-Clonal Deletion,
pubmed-meshheading:14707073-Diabetes Mellitus, Type 1,
pubmed-meshheading:14707073-Disease Models, Animal,
pubmed-meshheading:14707073-H-2 Antigens,
pubmed-meshheading:14707073-Hemagglutinin Glycoproteins, Influenza Virus,
pubmed-meshheading:14707073-Histocompatibility Antigens Class II,
pubmed-meshheading:14707073-Insulin,
pubmed-meshheading:14707073-Islets of Langerhans,
pubmed-meshheading:14707073-Mice,
pubmed-meshheading:14707073-Mice, Inbred C57BL,
pubmed-meshheading:14707073-Mice, Knockout,
pubmed-meshheading:14707073-Mice, Transgenic,
pubmed-meshheading:14707073-Promoter Regions, Genetic,
pubmed-meshheading:14707073-Rats,
pubmed-meshheading:14707073-Receptors, Antigen, T-Cell,
pubmed-meshheading:14707073-Thymus Gland
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pubmed:year |
2004
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pubmed:articleTitle |
In a transgenic model of spontaneous autoimmune diabetes, expression of a protective class II MHC molecule results in thymic deletion of diabetogenic CD8+ T cells.
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pubmed:affiliation |
University of Bristol, School of Medical Sciences, Bristol, United Kingdom.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|