Premium
Interleukin‐18 enhances HIV‐1 production in a human chronically‐infected T cell line (H9‐V)
Author(s) -
Pugliese Agostino,
Gennero Luisa,
Vidotto Valerio,
Speranza Filippo,
Tambini Roberto,
Torre Donato
Publication year - 2002
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.981
Subject(s) - cytokine , monoclonal antibody , cell culture , biology , stimulation , viral replication , interferon , t cell , virology , replication (statistics) , antibody , microbiology and biotechnology , immunology , immune system , endocrinology , genetics
Interleukin‐18 (IL‐18) is a recently identified immunoregulatory cytokine expressed by activated macrophages, that induces production of interferon‐γ (IFN‐γ) and Th‐1 development. Recently some investigators reported controversial in vitro data on IL‐18 stimulation of HIV‐1 replication in several cell lines. In the present study the effect of IL‐18 on HIV replication in a human chronically HIV‐1‐infected lymphocytic T cell line (H9‐V) was investigated. HIV‐1 replication was determined by an immunoassay method in order to evaluate the content of p24 antigen in the cell culture supernatants. Stimulation of H9‐V cells with IL‐18 resulted in increased production of p24, especially at concentrations of 0.01 μg ml −1 and 0.10 μg ml −1 . Moreover a significant and persistent IL‐18 stimulation of HIV‐1 replication was observed at a concentration of 0.01 μg ml −1 during a 7‐day period. Pre‐treatment of IL‐18 with a specific neutralizing monoclonal antibody significantly reduced HIV‐1 replication. These experiments show that IL‐18 promotes the increase of HIV‐1 replication in human chronically‐infected lymphocytic T cells and confirm the role of IL‐18 as a proimflammatory cytokine in stimulating and maintaining HIV‐1 replication during the course of the disease. In a successive set of experiments, since one of the main activities of IL‐18 is the induction of IFN‐γ, we evaluated the effect of this biological modifier on H9‐V cells. In particular, IFN‐γ shows a significant effect on cell replication and on reduction of CD4 and CD71 surface expression. Copyright © 2002 John Wiley & Sons, Ltd.