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Modulation of antigen processing by haem‐oxygenase 1. Implications on inflammation and tolerance
Author(s) -
Riquelme Sebastián A.,
Carreño Leandro J.,
Espinoza Janyra A.,
MackernOberti Juan Pablo,
AlvarezLobos Manuel M.,
Riedel Claudia A.,
Bueno Susan M.,
Kalergis Alexis M.
Publication year - 2016
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.12605
Subject(s) - inflammation , heme oxygenase , priming (agriculture) , immune system , immunity , immunology , t cell , antigen , biology , microbiology and biotechnology , heme , enzyme , biochemistry , botany , germination
Summary Haem‐oxygenase‐1 (HO‐1) is an enzyme responsible for the degradation of haem that can suppress inflammation, through the production of carbon 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 endotoxic 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 findings 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.