Linked Life Data

11440641

Source:http://linkedlifedata.com/resource/pubmed/id/11440641

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2001-7-6
pubmed:abstractText
Indoleamine 2,3-dioxygenase (IDO) is the rate-limiting enzyme in the catabolism of tryptophan. By creating a local microenvironment in which levels of tryptophan are low, IDO-expressing antigen-presenting cells (APC) could regulate T cell activation. This may be relevant to control both viral and bacterial replication as well as neoplastic cell growth. Interferon-alpha (IFN-alpha) is an antiviral cytokine affecting cellular differentiation. In addition, it reduces proliferation of CD4(+) T cells by several molecular mechanisms. To dissect the molecular steps responsible for the INF-mediated antiproliferative activity, we sought to determine whether activated primary CD4(+) T cells in the presence of IFN-alpha would produce IDO. We demonstrate here that IDO mRNA is not present in resting CD4(+) T cells. Stimulation with anti-CD3 plus interleukin-2 (IL-2) induces expression of IDO mRNA (about 2000 copies/150,000 cells), as determined by semiquantitative RT-PCR. When cells were stimulated in the presence of IFN-alpha, expression of IDO mRNA was significantly increased (more than 12,000 copies/150,000 cells). Functional analysis of IDO activity paralleled the results obtained with RT-PCR, demonstrating increased production of active enzyme in CD4(+) T cells stimulated in the presence of IFN-alpha. Our results indicate that IFN-alpha modulates levels of IDO produced by activated CD4(+) T cells. This would likely affect bystander cells by modifying levels of tryptophan in the local microenvironment.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1079-9907
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
431-7
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:11440641-Antigens, CD3, pubmed-meshheading:11440641-Base Sequence, pubmed-meshheading:11440641-CD4-Positive T-Lymphocytes, pubmed-meshheading:11440641-CD8-Positive T-Lymphocytes, pubmed-meshheading:11440641-Cells, Cultured, pubmed-meshheading:11440641-DNA Primers, pubmed-meshheading:11440641-Gene Expression, pubmed-meshheading:11440641-Humans, pubmed-meshheading:11440641-Indoleamine-Pyrrole 2,3,-Dioxygenase, pubmed-meshheading:11440641-Interferon-alpha, pubmed-meshheading:11440641-Kynurenine, pubmed-meshheading:11440641-Lymphocyte Activation, pubmed-meshheading:11440641-RNA, Messenger, pubmed-meshheading:11440641-Recombinant Proteins, pubmed-meshheading:11440641-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:11440641-Tryptophan, pubmed-meshheading:11440641-Tryptophan Oxygenase
pubmed:year
2001
pubmed:articleTitle
Human primary CD4 + T cells activated in the presence of IFN-alpha 2b express functional indoleamine 2,3-dioxygenase.
pubmed:affiliation
Institute of Human Virology, University of Maryland Biotechnology Institute (UMBI), Baltimore, MD 20201, USA.
pubmed:publicationType
Journal Article