HIV-1 matrix protein p17 prevents loss of CD28 expression during IL-2-induced maturation of naïve CD8(+) T cells.

Abstract:

: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.

journal_name

Viral Immunol

journal_title

Viral immunology

authors

Avolio M,Caracciolo S,Tosti G,Vollero L,Fiorentini S,Caruso A

doi

10.1089/vim.2007.0095

subject

Has Abstract

pub_date

2008-06-01 00:00:00

pages

189-202

issue

2

eissn

0882-8245

issn

1557-8976

journal_volume

21

pub_type

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