Source:http://linkedlifedata.com/resource/pubmed/id/14738151
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
11
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pubmed:dateCreated |
2004-1-23
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pubmed:abstractText |
Profound immune dysfunction is a constant feature in B-cell chronic lymphocytic leukemia (B-CLL) patients. Immunological abnormalities include hypogammaglobulinemia, impaired immunoglobulin class switching and diminished germinal center formation. This state of immune suppression renders B-CLL patients highly susceptible to infections, which contribute greatly to morbidity and mortality in this disease. Impaired T cell function in B-CLL is well-documented and has been suggested to result from inhibitory effects exerted by malignant B lymphocytes. Because the presence of leukemic cells may represent a major obstacle to efficient T cell activation, T lymphocytes were separated from CLL B cells, stimulated with phorbol 12-myristate 13-acetate (PMA) and ionomycin for 4h, and then cocultured with autologous leukemic B cells both at a 1:1 ratio or at the same ratio as in vivo for 24-40 h. CLL B cell expression of CD86 and CD95 was markedly upregulated using this approach, whereas CD80 expression was augmented only in a minority of patients; these effects were partially preserved even when preactivated T cells were rechallenged with CLL B cells at the same low T/B cell ratio as that observed in vivo. Finally, CD80 upregulation on CLL B cells appeared to be mainly dependent on CD40L-mediated stimulation, whereas CD86 and CD95 expression was efficiently augmented by soluble factors released by preactivated T lymphocytes. In conclusion, efficient activation of T lymphocytes in B-CLL may be achieved which, in turn, may result in enhanced antigen-presenting capacity and susceptibility to apoptosis of leukemic cells via CD86 and CD95 upregulation, respectively.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD80,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD86,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/CD40 Ligand,
http://linkedlifedata.com/resource/pubmed/chemical/CD86 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Ionomycin,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Tetradecanoylphorbol Acetate
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
1042-8194
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
44
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1963-71
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:14738151-Aged,
pubmed-meshheading:14738151-Aged, 80 and over,
pubmed-meshheading:14738151-Antigens, CD,
pubmed-meshheading:14738151-Antigens, CD80,
pubmed-meshheading:14738151-Antigens, CD86,
pubmed-meshheading:14738151-Antigens, CD95,
pubmed-meshheading:14738151-Apoptosis,
pubmed-meshheading:14738151-B-Lymphocytes,
pubmed-meshheading:14738151-CD40 Ligand,
pubmed-meshheading:14738151-Coculture Techniques,
pubmed-meshheading:14738151-Female,
pubmed-meshheading:14738151-Humans,
pubmed-meshheading:14738151-Immunophenotyping,
pubmed-meshheading:14738151-Ionomycin,
pubmed-meshheading:14738151-Leukemia, Lymphocytic, Chronic, B-Cell,
pubmed-meshheading:14738151-Lymphocyte Activation,
pubmed-meshheading:14738151-Male,
pubmed-meshheading:14738151-Membrane Glycoproteins,
pubmed-meshheading:14738151-Middle Aged,
pubmed-meshheading:14738151-T-Lymphocytes,
pubmed-meshheading:14738151-Tetradecanoylphorbol Acetate,
pubmed-meshheading:14738151-Up-Regulation
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pubmed:year |
2003
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pubmed:articleTitle |
Effects of preactivated autologous T lymphocytes on CD80, CD86 and CD95 expression by chronic lymphocytic leukemia B cells.
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pubmed:affiliation |
Division of Internal Medicine, Allergy and Clinical Immunology, Department of Gerontology, Geriatrics, and Metabolic Diseases, Second University of Naples School of Medicine, Piazza L. Miraglia, 3, 80138 Naples, Italy.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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