AUTHOR=Pérez-Mazliah Damián , Albareda María C., Alvarez María G., Lococo Bruno E., Bertocchi Graciela L., Petti Marcos , Viotti Rodolfo , Laucella Susana A.

TITLE=Allopurinol reduces antigen-specific and polyclonal activation of human T cells

JOURNAL=Frontiers in Immunology

VOLUME=3

YEAR=2012

URL=https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2012.00295

DOI=10.3389/fimmu.2012.00295

ISSN=1664-3224

ABSTRACT=<p>Allopurinol is the most popular commercially available xanthine oxidase inhibitor and it is widely used for treatment of symptomatic hyperuricaemia, or gout. Although, several anti-inflammatory actions of allopurinol have been demonstrated <italic>in vivo</italic> and <italic>in vitro</italic>, there have been few studies on the action of allopurinol on T cells. In the current study, we have assessed the effect of allopurinol on antigen-specific and mitogen-driven activation and cytokine production in human T cells. Allopurinol markedly decreased the frequency of IFN-γ and IL-2-producing T cells, either after polyclonal or antigen-specific stimulation with Herpes Simplex virus 1, Influenza (Flu) virus, tetanus toxoid and <italic>Trypanosoma cruzi</italic>-derived antigens. Allopurinol attenuated CD69 upregulation after CD3 and CD28 engagement and significantly reduced the levels of spontaneous and mitogen-induced intracellular reactive oxygen species in T cells. The diminished T cell activation and cytokine production in the presence of allopurinol support a direct action of allopurinol on human T cells, offering a potential pharmacological tool for the management of cell-mediated inflammatory diseases.</p>