Recovery of interleukin-17 production from interleukin-15-stimulated CD4+ mononuclear cells in HIV-1-infected patients with sustained viral suppression.

Published

Journal Article

Interleukin-17 (IL-17) is a pro-inflammatory cytokine that is mainly produced by CD4+ T cells. The role of Th17 during the human immunodeficiency virus (HIV)-1 infection is still unclear, but HIV-1 infection can cause a preferential depletion of Th17 cells. It has been shown that IL-15 elicits IL-17 production from human peripheral blood mononuclear cells. We studied the effect of IL-15 stimulation in vitro on IL-17 production from CD4+ mononuclear cells of HIV-infected patients. We observed that IL-15 triggers, in a dose-dependent manner, IL-17 secretion. This effect was blocked by anti-IL-15 monoclonal antibody (P=0.01). Interestingly, IL-17 production was significantly lower in patients with detectable plasma viremia when compared with successfully treated HIV-infected patients (P=0.02) and healthy controls, respectively (P<0.001). We also noticed a significant difference in IL-17 production between naïve HIV-infected patients and patients with virological failure on combined antiretroviral therapy (cART) (P=0.02). Our results suggest that IL-15 can induce IL-17 production from peripheral CD4+ mononuclear cells of HIV-infected patients. Persistent HIV plasma viremia could cause a severe perturbation of IL-17 production from CD4+ mononuclear cells. IL-17 production in HIV-infected patients could be recovered through a sustained suppression of the viral replication in the peripheral blood through cART.

Full Text

Duke Authors

Cited Authors

  • Zaffiri, L; d'Ettorre, G; Ceccarelli, G; Andreotti, M; Marcellini, S; Giustini, N; Ascoli-Bartoli, T; Mastroianni, CM; Vella, S; Vullo, V

Published Date

  • January 2014

Published In

Volume / Issue

  • 34 / 1

Start / End Page

  • 35 - 40

PubMed ID

  • 24102576

Pubmed Central ID

  • 24102576

Electronic International Standard Serial Number (EISSN)

  • 1557-7465

Digital Object Identifier (DOI)

  • 10.1089/jir.2012.0011

Language

  • eng

Conference Location

  • United States