Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1991-5-21
pubmed:abstractText
Aspirin-like drugs (ALD) enhance T cell proliferation by suppressing PG production in monocytes. Normal human T cells do not produce any eicosanoids. Therefore we studied whether ALD would affect purified T cells directly. We found that ALD enhanced the proliferation and IL-2 production of T cells in the absence of monocytes. This effect did not depend on arachidonic acid metabolism as no lipoxygenase products and only nonsuppressive levels of cyclooxygenase products were detected in T cell cultures. Several possible mechanisms of the ALD effect were ruled out including 1) enhanced mitogen binding, 2) induction of activation markers (IL-2R, transferrin receptor, HLA-DR) on the cell surface, 3) down-regulation of suppressor cells. ALD caused a rise in [Ca2+]i which appeared to reflect an influx of Ca2+ from the extracellular milieu and was more pronounced in CD4+ cells. The rise in intracellular levels of Ca2+, that is considered a necessary second messenger for T cell activation, may prime these cells for an enhanced response to mitogens. In addition, ALD increased T cell membrane fluidity but only at higher concentrations than those found to enhance proliferation. The pharmacologic effect of ALD on T cells presents a possible new immunoenhancing potential of these drugs and may have therapeutic use in immunosuppressed individuals.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Inflammatory Agents..., http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD8, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation..., http://linkedlifedata.com/resource/pubmed/chemical/Arachidonic Acid, http://linkedlifedata.com/resource/pubmed/chemical/Arachidonic Acids, http://linkedlifedata.com/resource/pubmed/chemical/Calcium, http://linkedlifedata.com/resource/pubmed/chemical/Diclofenac, http://linkedlifedata.com/resource/pubmed/chemical/Dinoprostone, http://linkedlifedata.com/resource/pubmed/chemical/Flurbiprofen, http://linkedlifedata.com/resource/pubmed/chemical/Indomethacin, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2, http://linkedlifedata.com/resource/pubmed/chemical/Phytohemagglutinins
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
146
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2553-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:1901879-Adult, pubmed-meshheading:1901879-Anti-Inflammatory Agents, Non-Steroidal, pubmed-meshheading:1901879-Antigens, CD8, pubmed-meshheading:1901879-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:1901879-Arachidonic Acid, pubmed-meshheading:1901879-Arachidonic Acids, pubmed-meshheading:1901879-Calcium, pubmed-meshheading:1901879-Cell Division, pubmed-meshheading:1901879-Chromatography, High Pressure Liquid, pubmed-meshheading:1901879-Diclofenac, pubmed-meshheading:1901879-Dinoprostone, pubmed-meshheading:1901879-Drug Synergism, pubmed-meshheading:1901879-Female, pubmed-meshheading:1901879-Flow Cytometry, pubmed-meshheading:1901879-Flurbiprofen, pubmed-meshheading:1901879-Humans, pubmed-meshheading:1901879-Indomethacin, pubmed-meshheading:1901879-Interleukin-2, pubmed-meshheading:1901879-Lymphocyte Activation, pubmed-meshheading:1901879-Male, pubmed-meshheading:1901879-Middle Aged, pubmed-meshheading:1901879-Phytohemagglutinins, pubmed-meshheading:1901879-Radioimmunoassay, pubmed-meshheading:1901879-T-Lymphocytes
pubmed:year
1991
pubmed:articleTitle
Aspirin-like drugs prime human T cells. Modulation of intracellular calcium concentrations.
pubmed:affiliation
Clinical Immunology Section, Audie L. Murphy Memorial Veterans Hospital, San Antonio, TX.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't