Riquelme, Sebastián A.Carreño, Leandro J.Espinoza, Janyra A.Mackern-Oberti, Juan PabloAlvarez-Lobos, Manuel M.Riedel, Claudia A.Bueno, Susan M.Kalergis, Alexis M.2023-09-272023-09-272016-09Immunology. Open Access. Volume 149, Issue 1, Pages 1 - 12. 1 September 20160019-2805https://repositorio.unab.cl/xmlui/handle/ria/53357Indexación: Scopus.Haem-oxygenase-1 (HO-1) is an enzyme responsible for the degradation of haem that can suppress inflammation, through the production of car bon monoxide (CO). It has been shown in several experimental models that genetic and pharmacological induction of HO-1, as well as non-toxic administration of CO, can reduce inflammatory diseases, such as endo toxic shock, type 1 diabetes and graft rejection. Recently, it was shown that the HO-1/CO system can alter the function of antigen-presenting cells (APCs) and reduce T-cell priming, which can be beneficial during immune-driven inflammatory diseases. The molecular mechanisms by which the HO-1 and CO reduce both APC- and T-cell-driven immunity are just beginning to be elucidated. In this article we discuss recent find ings related to the immune regulatory capacity of HO-1 and CO at the level of recognition of pathogen-associated molecular patterns and T-cell priming by APCs. Finally, we propose a possible regulatory role for HO-1 and CO over the recently described mitochondria-dependent immunity. These concepts could contribute to the design of new therapeutic tools for inflammation-based diseases.enAntigen PresentationCarbon MonoxideCytokineDendritic CellsHaem-Oxygenase 1Artículo10.1111/imm.12605