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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
1995-9-1
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pubmed:abstractText |
Immunization with the extracellular domain of TSH receptor (TSHR) led to the development of hyperthyroxinemia in BALB/cJ, but not C57BL/6J, SJL/J, and B10.BR, mice. Earlier, human studies had shown that thyroid-stimulating antibodies are predominantly of the immunoglobulin G1 (IgG1) subclass with a narrow specificity to TSHR, and antibodies that block thyroid function could be of any subclass with a broader specificity. Therefore, antibody responses in susceptible (BALB/cJ) and resistant (SJL/J) mice were characterized. There were no significant differences in the titers, relative affinities, or isotypes of antibodies against the TSHR. BALB/cJ and SJL/J sera reacted with 2 and 7 of 26 overlapping peptides from the extracellular domain of the TSHR. The ability of sera from BALB/cJ and SJL/J mice to block TSH binding to TSHR was reversed by 1 and 6 of the reactive peptides, respectively. BALB/cJ mice showed predominantly an IgG1 response against the TSHR and peptides, whereas SJL/J mice showed varying levels of all IgG subclasses. Although SJL/J sera reacted with peptides to which blocking antibodies bind, they did not show hypothyroidism, suggesting that their sera contained a mixture of blocking and stimulating antibodies that negated the effects of each other. In contrast, some TSHR-specific antibodies in BALB/cJ probably represented stimulating antibodies.
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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/Antibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin G,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulin Isotypes,
http://linkedlifedata.com/resource/pubmed/chemical/Immunoglobulins,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Thyrotropin,
http://linkedlifedata.com/resource/pubmed/chemical/Thyrotropin
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0013-7227
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
136
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3461-9
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:7628382-Animals,
pubmed-meshheading:7628382-Antibodies,
pubmed-meshheading:7628382-Antibody Formation,
pubmed-meshheading:7628382-Antibody Specificity,
pubmed-meshheading:7628382-Disease Susceptibility,
pubmed-meshheading:7628382-Female,
pubmed-meshheading:7628382-Hyperthyroxinemia,
pubmed-meshheading:7628382-Immunization,
pubmed-meshheading:7628382-Immunoglobulin G,
pubmed-meshheading:7628382-Immunoglobulin Isotypes,
pubmed-meshheading:7628382-Immunoglobulins,
pubmed-meshheading:7628382-Mice,
pubmed-meshheading:7628382-Mice, Inbred BALB C,
pubmed-meshheading:7628382-Mice, Inbred Strains,
pubmed-meshheading:7628382-Peptides,
pubmed-meshheading:7628382-Receptors, Thyrotropin,
pubmed-meshheading:7628382-Thyroid Gland,
pubmed-meshheading:7628382-Thyrotropin
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pubmed:year |
1995
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pubmed:articleTitle |
Thyrotropin receptor-specific antibodies in BALB/cJ mice with experimental hyperthyroxinemia show a restricted binding specificity and belong to the immunoglobulin G1 subclass.
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pubmed:affiliation |
Department of Microbiology and Immunology, University of Texas Medical Branch, Galveston 77555-1019, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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