Title |
Allopurinol reduces antigen-specific and polyclonal activation of human T cells
|
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Published in |
Frontiers in immunology, January 2012
|
DOI | 10.3389/fimmu.2012.00295 |
Pubmed ID | |
Authors |
Damián Pérez-Mazliah, María C. Albareda, María G. Alvarez, Bruno Lococo, Graciela L. Bertocchi, Marcos Petti, Rodolfo J. Viotti, Susana A. Laucella |
Abstract |
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 in vivo and in vitro, 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 Trypanosoma cruzi-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. |
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