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Gabriel Mestre,
Felipe Garcia,
Esteban Martinez,
Ana Milinkovic,
Anna Lopez,
Agathe León,
Borja Mora,
Roger Argelich, José Manuel Lozano,
José Peña,
José M Gatell,
Montserrat Plana
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ABSTRACT: Few data evaluating the NK cell profile during structured therapy interruption (STI) in chronic HIV-1 infection are available. Changes in NK cell percentages and KIR and NKG2A receptors were analyzed at baseline and after 2 years of follow-up in 121 patients on ART with CD4(+) >450 cells/ml and VL <200 copies/ml randomized in three arms according to the criteria employed to resume ART during STI: virological arm (VA n = 47, VL >30,000 copies/ml or CD4 <350 cells/ml), immunological arm (IA n = 37, CD4< 350 cells/ml), and a control arm (n = 37) in which ART was maintained. After 2 years of follow-up, a decrease in CD3(-)CD56(+) CD16(+) cell percentages in VA and IA patients, but not in CA patients, was observed. Those patients with higher decrease in CD3(-)CD56(+)CD16(+) cells had a higher decrease in CD4(+) cells (r = 0.35, p = 0.001) and higher increase in PVL (r = -0.26, p = 0.02). KIR and NKG2A receptor expression tended to increase in CA and decreased in the other two arms (more in IA than in VA). Patients who displayed a greater decrease in CD4(+) T cells and a greater rise in PVL after 2 years of follow-up had a significantly higher decrease in KIR and NKG2A receptors expressed in CD3(-)CD56(+) cells. Patients who presented the lowest levels of total NK cells and KIR and NKG2A receptor expression after STI showed the poorest virology or immunology outcomes. This finding suggests that STI could decrease the number of NK subsets, which is related to the worst clinical development in these patients.
AIDS research and human retroviruses 12/2008; 24(12):1485-95. · 2.18 Impact Factor
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ABSTRACT: In order to better understand the possible beneficial effects of intermittent IL-2 treatment as complement of antiretroviral therapy in HIV-1+ patients, we have measured the levels of RANTES in the supernatants and the CD25 expression in cultured PBMCs obtained from HIV-1+ individuals in presence of IL-2. The results showed a significant increases in RANTES production and in the expression of CD25+ in the cultures with IL-2 of PBMC obtained from HIV-1+ patients with a detectable viral load in comparison with both, HIV-1+ patients with no detectable viral loads and with healthy individuals. These results suggest that therapeutic IL-2 administered in addition to highly active anti-retroviral therapy (HAART) may contribute to increase the effect of this therapy by rising both RANTES production and CD25 expression only in HIV-1+ patients with detectable viral loads.
International Immunopharmacology 07/2006; 6(6):1034-8. · 2.38 Impact Factor
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Almudena Cabello,
Antonio Rivero,
Mariá José Garcia, José Manuel Lozano,
Julian Torre-Cisneros,
Rafael González,
Gema Dueñas,
Maria Dolores Galiani,
Angela Camacho,
Manuel Santamaria,
Rafael Solana,
Carmen Montero,
José Mariá Kindelán,
José Peña
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ABSTRACT: The aim of this work is to analyze if the highly active antiretroviral therapy (HAART) has any effect in the number of peripheral monocytes expressing the tolerogenic molecule human leukocyte antigen G (HLA-G) in HIV-1 infected individuals. In this sense, expression of HLA-G was measured by flow cytometry on peripheral monocytes from HIV-1 antiretroviral-receiving and antiretroviral naïve patients and in HIV-1 patients at different times after the antiretroviral treatments were removed. It was found an increment of monocytes expressing HLA-G in HIV-1 infected individuals receiving HAART, whereas monocytes from untreated HIV-1 patients did not change. When the HLA-G was measured on monocytes after antiretroviral treatment was removed, the number of peripheral monocytes expressing HLA-G was progressively decreasing. These data suggest that antiretroviral therapy is able to induce the expression of the tolerogenic molecule HLA-G on peripheral monocytes from HIV-1 seropositive individuals.
Human Immunology 12/2003; 64(11):1045-9. · 2.84 Impact Factor
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ABSTRACT: Tumour necrosis factor-alpha (TNF-alpha) mediates hepatocyte cell death by D-galactosamine (D-GalN) and its protection by prostaglandin E(1) (PGE(1)). The activation of immune system plays an important role in the development of liver injury. TNF-alpha and PGE(1) regulate the activity and cytokine release of different inflammatory cells. The present study was undertaken to determine if the noxious or hepatic protective properties of TNF-alpha during D-GalN-induced liver injury was related to an alteration by PGE(1) of the immunoregulatory activity of TNF-alpha. The role of TNF-alpha was assessed by anti-TNF-alpha antibodies to D-GalN-treated rats in the presence or absence of PGE(1). D-GalN enhanced the percentage of monocytes and T lymphocytes in the total peripheral blood mononuclear cells (PBMCs). D-GalN enhanced the activation degree of monocytes, but reduced that of T lymphocytes. D-GalN also enhanced TNF-alpha, IL-1alpha, IL-6 and IFN-gamma concentrations in blood. Anti-TNF-alpha antibodies abolished all immunological changes and greatly reduced liver damage induced by D-GalN. The protection by PGE(1) against D-GalN liver injury was associated with an increase in TNF-alpha concentration and a reduction of IL-1alpha and IL-6. These changes were associated with a reduction of monocyte activation degree and a recovery of that of T lymphocytes. Although anti-TNF-alpha antibodies abolished the protection by PGE(1) against D-GalN-liver injury, they did not essentially counteract the effect of the prostanoid in all immunological parameters studied. The present study showed that the protection against D-GalN liver damage by PGE(1) or anti-TNF-alpha was associated with similar effects on the inflammatory parameters studied. Nevertheless, the abolishment of liver protection by PGE(1) with anti-TNF-alpha in D-GalN-treated rats in the presence of a protective cytokine profile suggests that the release of TNF-alpha induced by PGE(1) pre-administration was exerting a direct protective effect on hepatocytes against D-GalN injury. Consequently, the effect of PGE(1) on inflammatory parameters studied during liver injury was unrelated to TNF-alpha.
International Immunopharmacology 03/2003; 3(2):197-207. · 2.38 Impact Factor
