Linked Life Data

10553102

Source:http://linkedlifedata.com/resource/pubmed/id/10553102

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1999-12-2
pubmed:abstractText
The low precursor frequency of Ag-reactive CD4+ T cells has been a barrier to the study of CD4+ T cell responses to conventional Ags as well as CD4+ T cell responses to autoantigens recognized during the course of an autoimmune disease. We have recently reported that all "conventional Ag" reactive CD4+ T cells are contained within the subpopulation expressing high levels of the CD4 molecule, termed CD4high. We have identified a CD4high population in the islets of Langerhans of prediabetic nonobese diabetic (NOD) mice that is extremely potent in transferring disease. As few as 500 CD4high islet-infiltrating CD4+ T cells transferred insulin-dependent diabetes mellitus to CD8 reconstituted NOD-SCID mice within 30 days of transfer. In contrast, CD4high T cells isolated from either NOD spleen or salivary glands did not transfer insulin-dependent diabetes mellitus into similar CD8-reconstituted NOD-SCID recipients. These data indicate that the precursor frequency of NOD islet-reactive, pathogenic CD4+ T cells is much higher in the prediabetic NOD pancreas than in these other organs. The islet-infiltrating CD4high T cells displayed selected memory markers, by cell surface analysis, and displayed a Th 1 phenotype by RNase protection assay, but had a marked decrease in IL-4 mRNA determined by quantitative real time PCR when compared with the less pathogenic CD4normal islet-infiltrating T cells. Use of the CD4high marker to select Ag activated T cells represents a tool to isolate and study pathogenic CD4+ T cells from autoimmune lesions in which the Ag has not been previously defined.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
163
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5708-14
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10553102-Animals, pubmed-meshheading:10553102-Antigens, CD4, pubmed-meshheading:10553102-Autoantigens, pubmed-meshheading:10553102-Biological Markers, pubmed-meshheading:10553102-CD4-Positive T-Lymphocytes, pubmed-meshheading:10553102-CD8-Positive T-Lymphocytes, pubmed-meshheading:10553102-Cell Movement, pubmed-meshheading:10553102-Cell Separation, pubmed-meshheading:10553102-Cytokines, pubmed-meshheading:10553102-Diabetes Mellitus, Type 1, pubmed-meshheading:10553102-Female, pubmed-meshheading:10553102-Immunologic Memory, pubmed-meshheading:10553102-Immunophenotyping, pubmed-meshheading:10553102-Interleukin-4, pubmed-meshheading:10553102-Islets of Langerhans, pubmed-meshheading:10553102-Islets of Langerhans Transplantation, pubmed-meshheading:10553102-Lymphocyte Count, pubmed-meshheading:10553102-Mice, pubmed-meshheading:10553102-Mice, Inbred NOD, pubmed-meshheading:10553102-Mice, SCID, pubmed-meshheading:10553102-Organ Specificity, pubmed-meshheading:10553102-Prediabetic State, pubmed-meshheading:10553102-Self Tolerance, pubmed-meshheading:10553102-Th1 Cells
pubmed:year
1999
pubmed:articleTitle
Isolation of self antigen-reactive cells from inflamed islets of nonobese diabetic mice using CD4high expression as a marker.
pubmed:affiliation
Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine, CA 94305, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't