Source:http://linkedlifedata.com/resource/pubmed/id/18570590
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rdf:type | |
lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0019704,
umls-concept:C0033684,
umls-concept:C0039194,
umls-concept:C0085358,
umls-concept:C0185117,
umls-concept:C0331858,
umls-concept:C1254042,
umls-concept:C1292733,
umls-concept:C1332709,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1422055,
umls-concept:C1517945,
umls-concept:C1704640,
umls-concept:C1706438,
umls-concept:C1706515,
umls-concept:C2698600,
umls-concept:C2911684
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pubmed:issue |
2
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pubmed:dateCreated |
2008-6-23
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pubmed:abstractText |
Naïve CD8(+) T cells differentiate into effectors secreting various cytokines that modulate immune functions. A striking finding for most HIV-1-infected patients is that they accumulate CD8(+) T cells belonging to early and intermediate differentiated elements. Structural HIV-1 proteins, and among these the matrix protein p17, have been associated with loss of functional competence by different immune cells. We therefore evaluated the influence of p17 on naïve CD8(+) T-cell activation and maturation. Anti-CD3 mAb preactivation and subsequent IL-2 stimulation are able to drive human naive CD(+) T cells to an effector phenotype characterized, among other features, by downregulation of the co-stimulatory molecule CD28. Strikingly, however, IL-2-induced downmodulation of CD28 was completely prevented by p17, and cells derived from p17-stimulated cultures showed a strong Tc1 polarization that was fourfold higher than that observed in IL-2-stimulated cultures.Moreover, p17 preserved a markedly high proportion of CD8(+) T cells that were able to respond to CD28 triggering with a proinflammatory cytokine storm. Our evidence suggests that p17 has important effects on cytokine polarization and phenotype of terminally differentiated CD8(+) T cells, and that new p17-based therapeutic approaches could control or prevent HIV-1-related immune disorders.
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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, CD28,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/HIV Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/gag Gene Products, Human...,
http://linkedlifedata.com/resource/pubmed/chemical/p17 protein, Human...
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0882-8245
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
21
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
189-202
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pubmed:meshHeading |
pubmed-meshheading:18570590-Antigens, CD28,
pubmed-meshheading:18570590-Antigens, CD3,
pubmed-meshheading:18570590-Cells, Cultured,
pubmed-meshheading:18570590-Flow Cytometry,
pubmed-meshheading:18570590-HIV Antigens,
pubmed-meshheading:18570590-HIV-1,
pubmed-meshheading:18570590-Humans,
pubmed-meshheading:18570590-Interleukin-2,
pubmed-meshheading:18570590-Lymphocyte Activation,
pubmed-meshheading:18570590-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:18570590-gag Gene Products, Human Immunodeficiency Virus
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pubmed:year |
2008
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pubmed:articleTitle |
HIV-1 matrix protein p17 prevents loss of CD28 expression during IL-2-induced maturation of naïve CD8(+) T cells.
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pubmed:affiliation |
Department of Experimental and Applied Medicine, Section of Microbiology, University of Brescia Medical School, Brescia, Italy.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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