pubmed-article:16087865 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16087865 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:16087865 | lifeskim:mentions | umls-concept:C0011854 | lld:lifeskim |
pubmed-article:16087865 | lifeskim:mentions | umls-concept:C0599779 | lld:lifeskim |
pubmed-article:16087865 | pubmed:issue | 33 | lld:pubmed |
pubmed-article:16087865 | pubmed:dateCreated | 2005-8-17 | lld:pubmed |
pubmed-article:16087865 | pubmed:abstractText | Mice deficient in programmed cell death 1 (PD-1, Pdcd1), an immunoinhibitory receptor belonging to the CD28/cytotoxic T lymphocyte-associated antigen-4 family, spontaneously develop lupus-like autoimmune disease and autoimmune dilated cardiomyopathy on C57BL/6 and BALB/c backgrounds, respectively. However, how PD-1 deficiency induces different forms of autoimmune diseases on these two strains was unknown. Here, we report that PD-1 deficiency specifically accelerates the onset and frequency of type I diabetes in NOD (nonobese diabetic) mice, with strong T helper 1 polarization of T cells infiltrating into islets. These results suggest that PD-1 deficiency accelerates autoimmune predisposition of the background strain, leading to the induction of different forms of autoimmune diseases depending on the genetic background of the strain. Using NOD-Pdcd1-/- mice as an efficient animal model of type I diabetes, we screened diabetes-susceptible loci by genetic linkage analysis. The diabetic incidence of NOD-Pdcd1-/- mice was controlled by five genetic loci, including three known recessive loci [Idd (insulin-dependent diabetes) 1, Idd17, and Idd20] and two previously unidentified dominant loci [Iddp (Idd under PD-1 deficiency) 1 and Iddp2]. | lld:pubmed |
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pubmed-article:16087865 | pubmed:language | eng | lld:pubmed |
pubmed-article:16087865 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16087865 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:16087865 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16087865 | pubmed:month | Aug | lld:pubmed |
pubmed-article:16087865 | pubmed:issn | 0027-8424 | lld:pubmed |
pubmed-article:16087865 | pubmed:author | pubmed-author:WangJianJ | lld:pubmed |
pubmed-article:16087865 | pubmed:author | pubmed-author:HonjoTasukuT | lld:pubmed |
pubmed-article:16087865 | pubmed:author | pubmed-author:HiaiHiroshiH | lld:pubmed |
pubmed-article:16087865 | pubmed:author | pubmed-author:OkazakiTakuT | lld:pubmed |
pubmed-article:16087865 | pubmed:author | pubmed-author:YoshidaTakuT | lld:pubmed |
pubmed-article:16087865 | pubmed:author | pubmed-author:NakakiFumioF | lld:pubmed |
pubmed-article:16087865 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16087865 | pubmed:day | 16 | lld:pubmed |
pubmed-article:16087865 | pubmed:volume | 102 | lld:pubmed |
pubmed-article:16087865 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16087865 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16087865 | pubmed:pagination | 11823-8 | lld:pubmed |
pubmed-article:16087865 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:16087865 | pubmed:year | 2005 | lld:pubmed |
pubmed-article:16087865 | pubmed:articleTitle | Establishment of NOD-Pdcd1-/- mice as an efficient animal model of type I diabetes. | lld:pubmed |
pubmed-article:16087865 | pubmed:affiliation | Department of Medical Chemistry and Molecular Biology, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Sakyo-ku, Kyoto 606-8501, Japan. | lld:pubmed |
pubmed-article:16087865 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16087865 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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