Linked Life Data

11244301

Source:http://linkedlifedata.com/resource/pubmed/id/11244301

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-3-13
pubmed:abstractText
Glucocorticoids inhibit stimulus-induced T-cell proliferation, an early and essential parameter of cellular immunity. It was recently found however that physiological concentrations of glucocorticoids can also accelerate, not only inhibit, rat T-cell mitogenesis. We investigated mechanism(s) underlying mitogenic actions of glucocorticoids on anti-T-cell receptor (TCR)- and concanavalin A (Con A)-induced T-cell proliferation. Surprisingly, the ability of the glucocorticoid corticosterone (CORT) to either enhance or inhibit T-cell proliferation was found to depend primarily on the cell density and the timing of the cultures. At cell densities up to 1 x 10(5) cells/well (i.e. 'low' density), CORT inhibited T-cell proliferation irrespective of the culture time. In contrast, at cell densities of 2 x 10(5) cells/well and higher ('high' density), CORT potently stimulated T-cell mitogenesis during the first 2-3 culture days, but subsequently inhibited the proliferative response after 5-7 days. The glucocorticoid receptor antagonist RU486 completely abolished the effects of CORT. However, production of the main T cell growth factor interleukin (IL)-2 was inhibited by CORT at both 'low' and 'high' cell densities. In addition, irrespective of cell density, T-cell mitogenesis under either control conditions or in presence of CORT was completely blocked by an anti-IL-2-receptor-alpha-chain (IL-2Ralpha) antibody, indicating that T-cell proliferation was dependent on the IL-2 pathway. Immunofluorescence staining of IL-2Ralpha on CD4+ cells after 2-3 days in culture was increased by CORT, but only on cells cultured at 'high' density. Thus, glucocorticoids increase T-cell responsiveness to IL-2 under conditions of 'high' cell density only. We conclude that glucocorticoids may contribute to a more efficient early stage of cellular immune responses under conditions of intimate cell-to-cell contact (i.e. 'high' cell density), a situation likely to be present in vivo, for instance in lymph nodes. Thus, these findings are relevant to our understanding of the glucocorticoid control of immune function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0028-3835
pubmed:author
pubmed:copyrightInfo
Copyright 2001 S. Karger AG, Basel.
pubmed:issnType
Print
pubmed:volume
73
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
139-48
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Bidirectional effects of corticosterone on splenic T-cell activation: critical role of cell density and culture time.
pubmed:affiliation
Max Planck Institute of Psychiatry, Section of Neuropsychopharmacology, Munich, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't