Source:http://linkedlifedata.com/resource/pubmed/id/10605017
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2000-1-19
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pubmed:abstractText |
The period that precedes onset of insulin-dependent diabetes mellitus corresponds to an active dynamic state in which pathogenic autoreactive T cells are kept from destroying beta cells by regulatory T cells. In prediabetic nonobese diabetic (NOD) mice, CD4+ splenocytes were shown to prevent diabetes transfer in immunodeficient NOD recipients. We now demonstrate that regulatory splenocytes belong to the CD4+ CD62Lhigh T cell subset that comprises a vast majority of naive cells producing low levels of IL-2 and IFN-gamma and no IL-4 and IL-10 upon in vitro stimulation. Consistently, the inhibition of diabetes transfer was not mediated by IL-4 and IL-10. Regulatory cells homed to the pancreas and modified the migration of diabetogenic to the islets, which resulted in a decreased insulitis severity. The efficiency of CD62L+ T cells was dose dependent, independent of sex and disease prevalence. Protection mechanisms did not involve the CD62L molecule, an observation that may relate to the fact that CD4+ CD62Lhigh lymph node cells were less potent than their splenic counterparts. Regulatory T cells were detectable after weaning and persist until disease onset, sustaining the notion that diabetes is a late and abrupt event. Thus, the CD62L molecule appears as a unique marker that can discriminate diabetogenic (previously shown to be CD62L-) from regulatory T cells. The phenotypic and functional characteristics of protective CD4+ CD62L+ cells suggest they are different from Th2-, Tr1-, and NK T-type cells, reported to be implicated in the control of diabetes in NOD mice, and may represent a new immunoregulatory population.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
1
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pubmed:volume |
164
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
240-7
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:10605017-Animals,
pubmed-meshheading:10605017-CD4-Positive T-Lymphocytes,
pubmed-meshheading:10605017-Cell Differentiation,
pubmed-meshheading:10605017-Cell Movement,
pubmed-meshheading:10605017-Cytokines,
pubmed-meshheading:10605017-Diabetes Mellitus, Type 1,
pubmed-meshheading:10605017-Female,
pubmed-meshheading:10605017-Immunophenotyping,
pubmed-meshheading:10605017-Islets of Langerhans,
pubmed-meshheading:10605017-Killer Cells, Natural,
pubmed-meshheading:10605017-L-Selectin,
pubmed-meshheading:10605017-Male,
pubmed-meshheading:10605017-Mice,
pubmed-meshheading:10605017-Mice, Inbred NOD,
pubmed-meshheading:10605017-Mice, SCID,
pubmed-meshheading:10605017-Spleen,
pubmed-meshheading:10605017-T-Lymphocyte Subsets,
pubmed-meshheading:10605017-Th2 Cells
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pubmed:year |
2000
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pubmed:articleTitle |
Characterization of peripheral regulatory CD4+ T cells that prevent diabetes onset in nonobese diabetic mice.
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pubmed:affiliation |
Centre National de la Recherche Scientifique, Unité Mixte de Recherche 8603, Université Paris V, Hôpital Necker, Paris, France. lepault@necker.fr
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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