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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1995-8-18
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0896-8411
pubmed:author
pubmed:issnType
Print
pubmed:volume
8
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
209-20
pubmed:dateRevised
2004-11-17
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
pubmed:year
1995
pubmed:articleTitle
Differences in adhesion markers, activation markers, and TcR in islet infiltrating vs. peripheral lymphocytes in the NOD mouse.
pubmed:affiliation
Applied Immune Sciences, Santa Clara, CA 95054, USA.
pubmed:publicationType
Journal Article