HIV-1 induces NALP3-inflammasome expression and interleukin-1β secretion in dendritic cells from healthy individuals but not from HIV-positive patients

Alessandra Pontillo, Lais T. Silva, Telma M. Oshiro, Claudia Finazzo, Sergio Crovella, Alberto J S Duarte

Research output: Contribution to journalArticlepeer-review

Abstract

Objective: NALP3-inflammasome is an innate mechanism, alternative to type-1 interferon, which is able to recognize nucleic acids and viruses in the cytoplasm and to induce pro-inflammatory response. Here, we hypothesized the involvement of inflammasome in the early defense against HIV-1 and in the full maturation of dendritic cells: for this, we evaluated the response of dendritic cells pulsed with HIV-1 in terms of inflammasome activation in healthy donors. Moreover, inflammasome response to HIV was evaluated in HIV-infected individuals. DESIGN AND Methods: Monocyte-derived dendritic cells isolated from 20 healthy individuals (HC-DC) and 20 HIV-1-infected patients (HIV-DC) were pulsed with alditrithiol-2-inactivated HIV-1. We then analyzed inflammasome genes expression and interleukin-1β (IL-1β) secretion. Results: In HC-DC, HIV-1 induced higher NLRP3/NALP3 mRNA expression compared with other inflammasome genes such as NALP1/NLRP1 or IPAF/NLRC4 (P

Original languageEnglish
Pages (from-to)11-18
Number of pages8
JournalAIDS (London, England)
Volume26
Issue number1
DOIs
Publication statusPublished - Jan 2 2012

Keywords

  • dendritic cells
  • HIV-1
  • immunotherapy
  • inflammasome
  • interleukin-1β
  • NALP3
  • vaccine

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

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