Linked Life Data

19327547

Source:http://linkedlifedata.com/resource/pubmed/id/19327547

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2009-3-30
pubmed:abstractText
Vitamin C is an essential micronutrient, which has been implicated in various biological processes, including immune response. In fact, in vivo administration of vitamin C modulates T cell proliferation and cytokine secretion. In this study, we analyzed the mechanism by which mouse T cells take up vitamin C, and whether this uptake directly affected T cell functions. T cells internalized more vitamin C when they were activated, due to enhanced glucose transporter (GLUT)-1 and GLUT-3 expression that persisted up to 48 h after activation. Blocking oxidation of ascorbic acid (the reduced form of vitamin C) in the culture medium with 1,4-dithio-threitol (DTT) almost completely inhibited the enhanced vitamin C uptake. The presence of vitamin C at low concentrations during in vitro T cell activation did not affect proliferation or cytokine secretion (IFN-gamma, TNF-alpha, or IL-4) in response to PMA/ionomycin. In contrast, high concentrations (0.25-0.5 mM) of vitamin C lowered cell viability, reduced thymidine uptake, and decreased cytokine secretion. In conclusion, activated T cells upregulated GLUT-1 and -3 to increase vitamin C uptake. They took up vitamin C mostly in its oxidized form, rarely in its reduced form. Application of vitamin C to T cells in vitro did not recapitulate previously reported in vivo responses to vitamin C, suggesting that in vivo, vitamin C modulates T cells indirectly through other components of the microenvironment.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1878-3279
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
214
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
311-20
pubmed:meshHeading
pubmed-meshheading:19327547-Animals, pubmed-meshheading:19327547-Ascorbic Acid, pubmed-meshheading:19327547-Biological Transport, pubmed-meshheading:19327547-Cell Proliferation, pubmed-meshheading:19327547-Cell Survival, pubmed-meshheading:19327547-Cytokines, pubmed-meshheading:19327547-Dehydroascorbic Acid, pubmed-meshheading:19327547-Dithiothreitol, pubmed-meshheading:19327547-Glucose Transporter Type 1, pubmed-meshheading:19327547-Glucose Transporter Type 3, pubmed-meshheading:19327547-Immunomagnetic Separation, pubmed-meshheading:19327547-Ionomycin, pubmed-meshheading:19327547-Lymphocyte Activation, pubmed-meshheading:19327547-Male, pubmed-meshheading:19327547-Mice, pubmed-meshheading:19327547-Mice, Inbred BALB C, pubmed-meshheading:19327547-Oxidation-Reduction, pubmed-meshheading:19327547-T-Lymphocytes, pubmed-meshheading:19327547-Tetradecanoylphorbol Acetate, pubmed-meshheading:19327547-Thymidine
pubmed:year
2009
pubmed:articleTitle
Vitamin C enters mouse T cells as dehydroascorbic acid in vitro and does not recapitulate in vivo vitamin C effects.
pubmed:affiliation
Department of Anatomy and Tumor Immunity Medical Research Center, Seoul National University College of Medicine, 28 Yongon-Dong, Chongno-Gu, Seoul 110-799, Republic of Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't