Linked Life Data

1534039

Source:http://linkedlifedata.com/resource/pubmed/id/1534039

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1992-6-25
pubmed:abstractText
The present study has examined the effect of GSH on two lines of IL-2-dependent activated killer cells, LAK cells and alpha CD3-activated killer (CD3-AK) cells. We found that GSH added during first 24 hr decreased the generation of LAK and CD3-AK cells from resting lymphocytes, whereas after 48 hr of activation, the addition of GSH increased the killer cell activity. In addition, BSO, an inhibitor of GSH biosynthesis, decreased the proliferation and cytotoxic activities of activated killer cells, and the inhibitory effect was reversed by GSH. These results indicate that GSH downregulates the generation of LAK or CD3-AK cells from resting lymphocytes, but it upregulates the further differentiation of preactivated killer cells. The effect of GSH thus varied with the state of activation of the killer cells. Culturing CD3-AK cells in GSH did not change the distribution of T cell subsets, did not affect the cells' ability to produce lymphokine (IL-2), and did not induce suppressor cells. One striking change as revealed by flow cytometry analysis was that the levels of IL-2 receptor and TCR (alpha/beta)-CD3 were reduced by 80 and 30%, respectively, after 48 hr culturing in GSH. Determination of the mRNA of IL-2 receptor suggests that a post-transcriptional block existed. It appears that the negative effect of GSH on the function of surface IL-2 receptors or T cell receptors on resting lymphocytes severely affected the signal transduction through these receptors and thus abrogated or reduced LAK or CD3-AK cell response. In contrast, for preactivated killer cells, upregulation by intracellular GSH of IL-2 utilization is a dominant effect, thus allowing further differentiation of these killer cells. Our results indicate that the balance between the activation signal (IL-2 or alpha CD3) and the immunoregulatory signal (induced by GSH) may determine the outcome of the immune response.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0008-8749
pubmed:author
pubmed:issnType
Print
pubmed:volume
142
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
40-53
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed-meshheading:1534039-Animals, pubmed-meshheading:1534039-Antigens, CD3, pubmed-meshheading:1534039-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:1534039-Buthionine Sulfoximine, pubmed-meshheading:1534039-Female, pubmed-meshheading:1534039-Genes, myc, pubmed-meshheading:1534039-Glutathione, pubmed-meshheading:1534039-Interleukin-2, pubmed-meshheading:1534039-Killer Cells, Lymphokine-Activated, pubmed-meshheading:1534039-Lymphocyte Activation, pubmed-meshheading:1534039-Mercaptoethanol, pubmed-meshheading:1534039-Methionine Sulfoximine, pubmed-meshheading:1534039-Mice, pubmed-meshheading:1534039-Mice, Inbred C57BL, pubmed-meshheading:1534039-Receptors, Antigen, T-Cell, pubmed-meshheading:1534039-T-Lymphocyte Subsets, pubmed-meshheading:1534039-Time Factors, pubmed-meshheading:1534039-Transcription, Genetic
pubmed:year
1992
pubmed:articleTitle
Dichotomy of glutathione regulation of the activation of resting and preactivated lymphocytes.
pubmed:affiliation
Division of Cancer Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.
pubmed:publicationType
Journal Article