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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2008-6-23
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0882-8245
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
189-202
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
HIV-1 matrix protein p17 prevents loss of CD28 expression during IL-2-induced maturation of naïve CD8(+) T cells.
pubmed:affiliation
Department of Experimental and Applied Medicine, Section of Microbiology, University of Brescia Medical School, Brescia, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't