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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2003-2-3
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pubmed:abstractText |
Pancreatic islets of Langerhans are enveloped by peri-islet Schwann cells (pSC), which express glial fibrillary acidic protein (GFAP) and S100beta. pSC-autoreactive T- and B-cell responses arise in 3- to 4-week-old diabetes-prone non-obese diabetic (NOD) mice, followed by progressive pSC destruction before detectable beta-cell death. Humans with probable prediabetes generate similar autoreactivities, and autoantibodies in islet-cell autoantibody (lCA) -positive sera co-localize to pSC. Moreover, GFAP-specific NOD T-cell lines transferred pathogenic peri-insulitis to NOD/severe combined immunodeficient (NOD/SCID) mice, and immunotherapy with GFAP or S100beta prevented diabetes. pSC survived in rat insulin promoter Iymphocytic choriomeningitis virus (rip-LCMV) glycoprotein/CD8+ T-cell receptor(gp) double-transgenic mice with virus-induced diabetes, suggesting that pSC death is not an obligate consequence of local inflammation and beta-cell destruction. However, pSC were deleted in spontaneously diabetic NOD mice carrying the CD8+/8.3 T-cell receptor transgene, a T cell receptor commonly expressed in earliest islet infiltrates. Autoimmune targeting of pancreatic nervous system tissue elements seems to be an integral, early part of natural type 1 diabetes.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1078-8956
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pubmed:author |
pubmed-author:AfifiyanFatemehF,
pubmed-author:BeckerDorothy JDJ,
pubmed-author:CheungRoy KRK,
pubmed-author:DoschH-MichaelHM,
pubmed-author:ElfordAlishaA,
pubmed-author:JackowskiGeorgeG,
pubmed-author:LauAmbroseA,
pubmed-author:LiXiaomaoX,
pubmed-author:OhashiPamelaP,
pubmed-author:SampsonAnastaziaA,
pubmed-author:SantamariaPereP,
pubmed-author:SongAihuaA,
pubmed-author:TsuiHubertH,
pubmed-author:WinerShawnS
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pubmed:issnType |
Print
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pubmed:volume |
9
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
198-205
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12539039-Animals,
pubmed-meshheading:12539039-Autoantibodies,
pubmed-meshheading:12539039-Base Sequence,
pubmed-meshheading:12539039-DNA Primers,
pubmed-meshheading:12539039-Diabetes Mellitus, Type 1,
pubmed-meshheading:12539039-Female,
pubmed-meshheading:12539039-Fluorescent Antibody Technique,
pubmed-meshheading:12539039-Glial Fibrillary Acidic Protein,
pubmed-meshheading:12539039-Islets of Langerhans,
pubmed-meshheading:12539039-Male,
pubmed-meshheading:12539039-Mice,
pubmed-meshheading:12539039-Mice, Inbred Strains,
pubmed-meshheading:12539039-Nerve Growth Factors,
pubmed-meshheading:12539039-S100 Proteins,
pubmed-meshheading:12539039-Schwann Cells,
pubmed-meshheading:12539039-Species Specificity
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pubmed:year |
2003
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pubmed:articleTitle |
Autoimmune islet destruction in spontaneous type 1 diabetes is not beta-cell exclusive.
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pubmed:affiliation |
Hospital For Sick Children, Research Institute and Department of Pediatrics and Immunology, University of Toronto, Toronto, Ontario, Canada.
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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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