Source:http://linkedlifedata.com/resource/pubmed/id/11129116
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2000-12-20
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pubmed:abstractText |
H2 and HLA transgenes were utilized to clarify the role of class II genes in susceptibility to experimental autoimmune thyroiditis (EAT), a model for Hashimoto's thyroiditis (HT). Susceptibility was transferred by H2 class II transgenes to a resistant haplotype and by HLA-DRA/DRB1*0301 (DR3) transgene into class II-negative Ab0 mice. Mice with a HLA-DRB1*1502 (DR2) transgene remain resistant to mouse thyroglobulin (mTg)-induced EAT, illustrating the role of HLA-DRB1 polymorphism. A role for HLA-DQ polymorphism was shown with hTg-induced EAT in HLA-DQ*0301/DQB1*0302 (DQ8), but not HLA-DQ*0103/DQB1*0601 (DQ6), transgenic mice. Yet, both DQ8+ and DQ6+ mice were unresponsive to mTg. Single transgenes obviate the problems from DR/DQ linkage disequilibrium and may distinguish the degree of susceptibility and the response to shared or specific epitopes. The introduction of conserved Eak transgene into Ab0 mice reveals a new role for H2E molecules in EAT. Without H2A molecules, EalphaEbetab molecules and T cells respond to hTg or pTg with severe thyroiditis, but not to mTg, thus distinguishing self from nonself. However, IAb genes in resistant mice ameliorate Eak transgene-mediated thyroiditis, similar to the effect of Eak transgene on IAs-mediated EAT. Studies in HLA DQ/DR double transgenic mice simulating human haplotypes could reveal HLA class II gene interactions in HT.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:issn |
0883-0185
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
19
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
573-85
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11129116-Animals,
pubmed-meshheading:11129116-Disease Models, Animal,
pubmed-meshheading:11129116-Disease Susceptibility,
pubmed-meshheading:11129116-Gene Transfer Techniques,
pubmed-meshheading:11129116-H-2 Antigens,
pubmed-meshheading:11129116-Histocompatibility Antigens Class II,
pubmed-meshheading:11129116-Humans,
pubmed-meshheading:11129116-Mice,
pubmed-meshheading:11129116-Mice, Transgenic,
pubmed-meshheading:11129116-Polymorphism, Genetic,
pubmed-meshheading:11129116-Thyroglobulin,
pubmed-meshheading:11129116-Thyroiditis, Autoimmune,
pubmed-meshheading:11129116-Transgenes
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pubmed:year |
2000
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pubmed:articleTitle |
New revelations in susceptibility to autoimmune thyroiditis by the use of H2 and HLA class II transgenic models.
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pubmed:affiliation |
Department of Immunology and Microbiology, Wayne State University School of Medicine, Detroit MI 48201, USA. ykong@med.wayne.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Review
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