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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1995-8-18
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pubmed:abstractText |
Insulin dependent diabetes mellitus (IDDM) in the non-obese diabetic (NOD) mouse is the result of a cellular mediated autoimmune event that destroys pancreatic islet beta cells. This destruction is characterized by a progressive lymphocytic infiltration into the islets as well as circulating autoantibodies and T cells reactive with islet antigens. To gain a better understanding of the cells responsible for islet destruction we isolated lymphocytes from the islets of prediabetic NOD mice and conducted a comparative phenotypic analysis with the analogous subpopulations of lymphocytes isolated from peripheral blood and lymph node (LN) of the same mice. CD3+ cells were analysed for T cell receptor (TcR); cell bearing gamma delta TcR were consistently observed at a higher frequency in the infiltrating T cells than in the periphery. Lymphocytes were also characterized for the expression of CD4 and CD8 T cell markers and, within each population, for the expression of activation markers (CD25, CD69) and adhesion markers (CD51, CD54, CD11b, CD49e, L-selectin). Significantly increased levels of CD4+CD8+ double-positive and CD4-CD8- double-negative T cell populations were observed in the infiltrating lymphocytes as compared with peripheral lymphocytes. In addition, within both CD4 and CD8 subpopulations isolated from islet infiltrates, CD11b+ and CD49e+ cells were increased with respect to the same subset of cells isolated from the periphery. In contrast, the level of cells that expressed L-selectin was significantly higher in the periphery for both CD4+ and CD8+ cells than for infiltrating cells. These data describe the phenotype of islet reactive T cells in the NOD mouse and identify possible targets for therapeutic intervention.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/Biological Markers,
http://linkedlifedata.com/resource/pubmed/chemical/Cell Adhesion Molecules,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0896-8411
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
209-20
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:7612149-Animals,
pubmed-meshheading:7612149-Antigens, CD,
pubmed-meshheading:7612149-Antigens, Differentiation, B-Lymphocyte,
pubmed-meshheading:7612149-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:7612149-Autoimmune Diseases,
pubmed-meshheading:7612149-Biological Markers,
pubmed-meshheading:7612149-Cell Adhesion Molecules,
pubmed-meshheading:7612149-Cell Movement,
pubmed-meshheading:7612149-Diabetes Mellitus, Type 1,
pubmed-meshheading:7612149-Disease Models, Animal,
pubmed-meshheading:7612149-Endothelium, Vascular,
pubmed-meshheading:7612149-Female,
pubmed-meshheading:7612149-Immunity, Cellular,
pubmed-meshheading:7612149-Islets of Langerhans,
pubmed-meshheading:7612149-Lymphocyte Activation,
pubmed-meshheading:7612149-Lymphocyte Count,
pubmed-meshheading:7612149-Lymphocyte Subsets,
pubmed-meshheading:7612149-Mice,
pubmed-meshheading:7612149-Mice, Inbred NOD,
pubmed-meshheading:7612149-Receptors, Antigen, T-Cell
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pubmed:year |
1995
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pubmed:articleTitle |
Differences in adhesion markers, activation markers, and TcR in islet infiltrating vs. peripheral lymphocytes in the NOD mouse.
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pubmed:affiliation |
Applied Immune Sciences, Santa Clara, CA 95054, USA.
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pubmed:publicationType |
Journal Article
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