Source:http://linkedlifedata.com/resource/pubmed/id/16263243
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2005-11-21
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pubmed:abstractText |
To improve the feasibility of in vivo monitoring of autoreactive T cells in the diabetogenic process, we generated T1 and T2 doubly transgenic non-obese diabetic (NOD) mice in which transgenic human CD90 (hCD90) is simultaneously expressed on IFN-gamma-producing cells or murine CD90.1 (mCD90.1) is expressed on IL-4-producing cells. These transgenic NOD mice develop diabetes with the same kinetics and incidence as wild type NOD mice, permitting the physiological characterization of CD4(+)hCD90(+) cells, which represent T(H)1 cells in lymphoid organs and at the site of insulitis. CD4(+)hCD90(+) cells had a higher capacity to secret IFN-gamma than CD4(+)hCD90(-) cells in an autoantigen-specific manner. Transgenic mice treated with GAD65 plasmid were protected from autoimmune diabetes, and had a lower number of CD4(+)hCD90(+) cells, confirming the pathogenic role of CD4(+)hCD90(+) cells in autoimmune diabetes. To further investigate the effect of IL-12 on the development of T(H)1 cells in autoimmune diabetes, we crossed these doubly transgenic mice to IL-12p35-deficient NOD mice. Despite severe disturbance of diabetes in p35(-/-) mice, the frequency of T(H)1 cells in these mice was slightly lower than in wild type mice. These data support the pathological role of IL-12 in autoimmune diabetes and suggest the existence an IL-12-independent pathway of T(H)1 development.
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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:month |
Nov
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pubmed:issn |
0896-8411
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pubmed:author |
pubmed-author:ChangHsiu-YingHY,
pubmed-author:ChangTsung-HsienTH,
pubmed-author:HsiehShie-LiangSL,
pubmed-author:HungJung-TungJT,
pubmed-author:KungJohn TJT,
pubmed-author:LiaoJen-HsiangJH,
pubmed-author:LinYu-ChungYC,
pubmed-author:McDevittHughH,
pubmed-author:SytwuHuey-KangHK,
pubmed-author:WuShu-FenSF
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pubmed:issnType |
Print
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pubmed:volume |
25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
181-92
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pubmed:meshHeading |
pubmed-meshheading:16263243-Animals,
pubmed-meshheading:16263243-Antigens, Thy-1,
pubmed-meshheading:16263243-Diabetes Mellitus, Type 1,
pubmed-meshheading:16263243-Disease Models, Animal,
pubmed-meshheading:16263243-Female,
pubmed-meshheading:16263243-Humans,
pubmed-meshheading:16263243-Interleukin-12,
pubmed-meshheading:16263243-Kinetics,
pubmed-meshheading:16263243-Male,
pubmed-meshheading:16263243-Mice,
pubmed-meshheading:16263243-Mice, Inbred BALB C,
pubmed-meshheading:16263243-Mice, Inbred C57BL,
pubmed-meshheading:16263243-Mice, Inbred NOD,
pubmed-meshheading:16263243-Mice, Transgenic,
pubmed-meshheading:16263243-Plasmids,
pubmed-meshheading:16263243-Th1 Cells,
pubmed-meshheading:16263243-Th2 Cells
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pubmed:year |
2005
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pubmed:articleTitle |
Immunopathogenic role of TH1 cells in autoimmune diabetes: evidence from a T1 and T2 doubly transgenic non-obese diabetic mouse model.
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pubmed:affiliation |
Graduate Institute of Life Sciences, National Defense Medical Center, 161, Section 6, MinChuan East Road, Neihu, Taipei 114, Taiwan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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