Increased Level of Arginase Activity Correlates with Disease Severity in HIV-Seropositive Patients

Infection with human immunodeficiency virus (HIV) results in a chronic infection that progressively impairs the immune system. Although depletion of CD4+ T cells is frequently used to explain immunosuppression, chronicity of infection and progressive loss of CD4+ T cells are not sufficient to fully...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:The Journal of infectious diseases 2010-08, Vol.202 (3), p.374-385
Hauptverfasser: Cloke, T. E., Garvey, L., Choi, B.-S., Abebe, T., Hailu, A., Hancock, M., Kadolsky, U., Bangham, C. R. M., Munder, M., Müller, I., Taylor, G. P., Kropf, P.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Infection with human immunodeficiency virus (HIV) results in a chronic infection that progressively impairs the immune system. Although depletion of CD4+ T cells is frequently used to explain immunosuppression, chronicity of infection and progressive loss of CD4+ T cells are not sufficient to fully account for immune dysregulation. Arginase-induced l-arginine deprivation is emerging as a key mechanism for the down-regulation of immune responses. Here, we hypothesized that the level of arginase activity increases with disease severity in HIV-seropositive patients. We determined the levels of arginase activity in peripheral blood mononuclear cells from HIV-seropositive patients and uninfected control participants. Our results show that peripheral blood mononuclear cells from HIV-seropositive patients with low CD4+ T cell counts expressed statistically significantly higher levels of arginase activity, compared with patients with high CD4+ T cell counts or uninfected control participants. Furthermore, we found a statistically significant correlation between high level of arginase activity and high viral load in HIV-seropositive patients.
ISSN:0022-1899
1537-6613
DOI:10.1086/653736