@Article{,
AUTHOR = {Agostino Pugliese, Valerio Vidotto, Tiziana Beltramo, Donato Torre},
TITLE = {Regulation of interleukin-18 by THP-1 monocytoid cells stimulated with HIV-1 and Nef viral protein},
JOURNAL = {European Cytokine Network},
VOLUME = {16},
YEAR = {2005},
NUMBER = {3},
PAGES = {186--190},
URL = {http://www.techscience.com/ECN/v16n3/66211},
ISSN = {1952-4005},
ABSTRACT = {Interleukin (IL)-18 is a proinflammatory cytokine that plays an important role in both innate and
adaptive immune responses against several infectious pathogens. Relatively little is known about its production in
HIV-1 infection, and there are controversial data on the influence of IL-18 on HIV-1 replication in vitro. In this
study, we investigated the effect of HIV-1 infection, and challenge with recombinant HIV-1 proteins, on IL-18
production by THP-1 cells. This is a monocytoid cell line spontaneously producing IL-18, and consequently is
particularly suitable for the study of HIV-1 effects on this type of cytokine regulation. The results reported here
demonstrate a significant reduction in IL-18 secretion during HIV-infection. In fact, low levels of IL-18 were
released until 120 h from viral challenge (15 ± 11pg/mL at 24 h and 17 ± 13 at 96 h and < 12.5 at 120 h), whereas
IL-18 production by uninfected control cells was 193 ± 104pg/mL and 214 ± 114 pg/mL at 24 h and 120 h
respectively. At 168 h of incubation, IL-18 production by infected and uninfected cells was found to be 164 ± 88
pg/mL and 325 ± 101 pg/mL respectively (p = 0.001). Of the following viral proteins: gp 120, p24 and Nef, only the
last one induced decreased IL-18 secretion in the supernatants of THP-1 cells. This effect is more evident with the
concentrations of 5 –1.25 lg/mL of Nef protein (p < 0.0001). In conclusion, our data show that HIV-1 and its
regulatory protein, Nef, are able to down-regulate the release of IL-18, in vitro. These results confirm that a variety
of modulating effects on the immune response, induced by HIV-infection, may facilitate progression of HIV-1
infection.},
DOI = {}
}