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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 |
2005-10-19
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pubmed:abstractText |
The importance of dendritic cells (DC) in the activation of T cells and in the maintenance of self-tolerance is well known. We investigated whether alterations in phenotype and function of DC may contribute to the pathogenesis of Type 1 diabetes (T1DM). Mature DC (mDC) from 18 children with T1DM and 10 age-matched healthy children were tested. mDC, derived from peripheral blood monocytes cultured for 6 days in presence of interleukin (IL)-4 and granulocyte-macrophage colony stimulating factor (GM-CSF) and stimulated with lipopolysaccharide (LPS) for the last 24 h, were phenotyped for the expression of the co-stimulatory molecules B7.1 and B7.2. In six patients and six controls allogenic mixed leucocyte reaction (AMLR) was performed using mDC and cord blood-derived naive T cells at a DC/T naive ratio of 1 : 200. Proliferation was assessed on day 7 by [(3)H]-thymidine incorporation assay. Mature DC derived from patients showed, compared with controls, a reduced expression of B7.1 [mean of fluorescence intensity (MFI): 36.2 +/- 14.3 versus 72.9 +/- 34.5; P = 0.004] and B7.2 (MFI: 122.7 +/- 67.5 versus 259.6 +/- 154.1; P = 0.02). We did not find differences in the HLA-DR expression (P = 0.07). Moreover, proliferative response of allogenic naive T cells cultured with mDC was impaired in the patients (13471 +/- 9917.2 versus 40976 +/- 24527.2 cpm, P = 0.04). We also measured IL-10 and IL-12 concentration in the supernatant of DC cultures. Interestingly, we observed in the patients a sevenfold higher level of IL-10 (P = 0.07) and a ninefold lower level of IL-12 (P = 0.01). Our data show a defect in the expression of the co-stimulatory molecules and an impairment of DC priming function, events that might contribute to T1DM pathogenesis.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-10679081,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-10795741,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-10837075,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-11375417,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-11825563,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-11910893,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-12742378,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-12766766,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-14592922,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-14679045,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-15210771,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-1896073,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-3496540,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-3517648,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-7519245,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-7532678,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-7546405,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-7584144,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-7589143,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-8450229,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-8452815,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-8717514,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-9295017,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-9366401,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-9449722,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-9583742,
http://linkedlifedata.com/resource/pubmed/commentcorrection/16232222-9725265
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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 |
Nov
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pubmed:issn |
0009-9104
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
142
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
341-6
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:16232222-Adolescent,
pubmed-meshheading:16232222-Antigens, CD80,
pubmed-meshheading:16232222-Antigens, CD86,
pubmed-meshheading:16232222-Cells, Cultured,
pubmed-meshheading:16232222-Child,
pubmed-meshheading:16232222-Child, Preschool,
pubmed-meshheading:16232222-Dendritic Cells,
pubmed-meshheading:16232222-Diabetes Mellitus, Type 1,
pubmed-meshheading:16232222-Female,
pubmed-meshheading:16232222-Humans,
pubmed-meshheading:16232222-Immunophenotyping,
pubmed-meshheading:16232222-Infant,
pubmed-meshheading:16232222-Interleukin-10,
pubmed-meshheading:16232222-Interleukin-12,
pubmed-meshheading:16232222-Lymphocyte Activation,
pubmed-meshheading:16232222-Lymphocyte Culture Test, Mixed,
pubmed-meshheading:16232222-Male,
pubmed-meshheading:16232222-Self Tolerance,
pubmed-meshheading:16232222-T-Lymphocytes
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pubmed:year |
2005
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pubmed:articleTitle |
Altered phenotype and function of dendritic cells in children with type 1 diabetes.
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pubmed:affiliation |
Department of Pediatrics, Tor Vergata University, Rome, Italy. angelini@med.uniroma2.it
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pubmed:publicationType |
Journal Article
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