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|Title:||Allopurinol reduces antigen-specific and polyclonal activation of human T cells||Authors:||Pérez-Mazliah, Damián E
Albareda, María C
Alvarez, María G
Bertocchi, Graciela L
Viotti, Rodolfo J
Laucella, Susana A.
|Keywords:||Antiinflamatorios;Linfocitos T;Th1 cytokines;Alopurinol;Xantina Oxidasa||Issue Date:||2012||Journal:||Frontiers in immunology||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.
|Appears in Collections:||Publicaciones INP|
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