Linked Life Data

11675346

Source:http://linkedlifedata.com/resource/pubmed/id/11675346

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2001-10-24
pubmed:abstractText
Despite thymic deletion of cells with specificity for self-antigens, autoreactive T cells are readily detectable in the normal T-cell repertoire. In recent years, a population of CD4(+) T cells that constitutively express the interleukin-2 receptor-alpha chain, CD25, has been shown to play a pivotal role in the maintenance of self-tolerance in rodent models. This study investigated whether such a regulatory population exists in humans. A population of CD4(+)CD25(+) T cells, taken from the peripheral blood of healthy individuals and phenotypically distinct from recently activated CD4(+) T cells, was characterized. These cells were hyporesponsive to conventional T-cell stimuli and capable of suppressing the responses of CD4(+)CD25(-) T cells in vitro. Addition of exogenous interleukin-2 abrogated the hyporesponsiveness and suppressive effects of CD4(+)CD25(+) cells. Suppression required cell-to-cell contact but did not appear to be via the inhibition of antigen-presenting cells. In addition, there were marked changes in the expression of Notch pathway molecules and their downstream signaling products at the transcriptional level, specifically in CD4(+)CD25(+) cells, suggesting that this family of molecules plays a role in the regulatory function of CD4(+)CD25(+) cells. Cells with similar phenotype and function were detected in umbilical venous blood from healthy newborn infants. These results suggest that CD4(+)CD25(+) cells represent a population of regulatory T cells that arise during fetal life. Comparison with rodent CD4(+)CD25(+) cells suggests that this population may play a key role in the prevention of autoimmune diseases in humans.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
98
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2736-44
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11675346-Adult, pubmed-meshheading:11675346-Antigen-Presenting Cells, pubmed-meshheading:11675346-Autoimmune Diseases, pubmed-meshheading:11675346-CD4-Positive T-Lymphocytes, pubmed-meshheading:11675346-Cell Communication, pubmed-meshheading:11675346-Cell Culture Techniques, pubmed-meshheading:11675346-Fetal Blood, pubmed-meshheading:11675346-Humans, pubmed-meshheading:11675346-Infant, Newborn, pubmed-meshheading:11675346-Interleukin-2, pubmed-meshheading:11675346-Lymphocyte Activation, pubmed-meshheading:11675346-Membrane Proteins, pubmed-meshheading:11675346-Phytohemagglutinins, pubmed-meshheading:11675346-Receptor, Notch1, pubmed-meshheading:11675346-Receptors, Cell Surface, pubmed-meshheading:11675346-Receptors, Interleukin-2, pubmed-meshheading:11675346-Self Tolerance, pubmed-meshheading:11675346-Signal Transduction, pubmed-meshheading:11675346-T-Lymphocyte Subsets, pubmed-meshheading:11675346-Transcription, Genetic, pubmed-meshheading:11675346-Transcription Factors
pubmed:year
2001
pubmed:articleTitle
Human CD4(+)CD25(+) cells: a naturally occurring population of regulatory T cells.
pubmed:affiliation
Department of Immunology, Hammersmith Campus, Imperial College School of Medicine, London, United Kingdom.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't