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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1992-2-18
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pubmed:abstractText |
Patients harboring a malignant brain tumor have been described as being highly immunosuppressed, as evidenced by reduced numbers of T cells and the decreased ability of their lymphocytes to produce interleukin-2 (IL-2). In order to determine whether an intrinsic abnormality exists in the T lymphocytes of glioma patients and to evaluate what role corticosteroids may play in glioma-associated immunosuppression, in vitro T cell proliferative function in the presence of recombinant IL-2 (rIL-2) was examined in age-matched groups of normal control subjects, steroid-free patients with glial tumors, steroid-dependent patients with glial tumors, and steroid-dependent patients with nonglial cerebral tumors. The results demonstrated that, when enriched T cell populations of all brain-tumor patients were stimulated with rIL-2 and phytohemagglutinin (PHA), there were no statistically significant differences between any groups. In contrast, when T cell populations were stimulated with mitogenic combinations of phorbol ester, calcium ionophore, and rIL-2, those from steroid-dependent patients with glial tumors had a significantly lower response than those from normal control subjects, suggesting that a population of T cells capable of responding to phorbol ester/ionomycin and not PHA stimulation is inhibited by corticosteroid therapy in glioma patients. In addition, T cells of four brain-tumor patient/age-matched control subject pairs were stimulated with either phorbol ester/ionomycin or PHA for 24 hours; three of the four patients expressed low-affinity IL-2 receptor levels as high or higher than their respective control subjects, suggesting that IL-2 receptor expression in these patients may be quantitatively normal once the T cell number is corrected. Taken together, these results show that the decreased PHA responsiveness that has been previously reported in lymphocytes of glioma patients is not due to a cellular abnormality within the potentially responsive cells, but rather reflects the reduced proportion of T cells within their peripheral blood which, as a consequence, reduces the level of IL-2 production attained upon activation.
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pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adrenal Cortex Hormones,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Ionomycin,
http://linkedlifedata.com/resource/pubmed/chemical/Phorbol 12,13-Dibutyrate,
http://linkedlifedata.com/resource/pubmed/chemical/Phytohemagglutinins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0022-3085
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
76
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
251-60
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1730954-Adrenal Cortex Hormones,
pubmed-meshheading:1730954-Adult,
pubmed-meshheading:1730954-Aged,
pubmed-meshheading:1730954-Brain Neoplasms,
pubmed-meshheading:1730954-Female,
pubmed-meshheading:1730954-Glioma,
pubmed-meshheading:1730954-Humans,
pubmed-meshheading:1730954-Immune Tolerance,
pubmed-meshheading:1730954-Interleukin-2,
pubmed-meshheading:1730954-Ionomycin,
pubmed-meshheading:1730954-Lymphocyte Activation,
pubmed-meshheading:1730954-Male,
pubmed-meshheading:1730954-Middle Aged,
pubmed-meshheading:1730954-Phorbol 12,13-Dibutyrate,
pubmed-meshheading:1730954-Phytohemagglutinins,
pubmed-meshheading:1730954-Receptors, Interleukin-2,
pubmed-meshheading:1730954-Recombinant Proteins,
pubmed-meshheading:1730954-T-Lymphocytes,
pubmed-meshheading:1730954-Tumor Cells, Cultured
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pubmed:year |
1992
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pubmed:articleTitle |
In vitro analysis of the proliferative potential of T cells from patients with brain tumor: glioma-associated immunosuppression unrelated to intrinsic cellular defect.
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pubmed:affiliation |
Department of Anatomy, Virginia Commonwealth University, Medical College of Virginia, Richmond.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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