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Increased Tryptophan (Trp) catabolism via the Kynurenine (Kyn) pathway is observed in several chronic inflammatory and infectious diseases, and is caused by increased indoleamine 2,3-dioxygenase (IDO) activity. In the particular case of HIV-1 infection, IDO dysregulation is considered to contribute to different aspects of immunopathogenesis, including immune deficiency, neurological impairment and tissue fibrosis. Increased IDO activity may result from direct activation of certain immune cell subsets by HIV (eg. plasmacytoid dendritic cell; pDC), or may be driven by the generalized immune activation observed during chronic HIV infection via inflammatory cytokines (such as type I and type II interferons) and ligand-receptor interactions (eg. binding of cytotoxic T lymphocyte antigen (CTLA)-4 to its ligands B7.1 and B7.2). Immunotherapeutic approaches which target IDO directly or indirectly are being considered for the treatment of HIV infection and have been tested mainly at preclinical level. The competitive IDO inhibitor 1-methyl-D-tryptophan (D-1mT) has been tested in both humanized mice and SIV/macaques with encouraging results, indicating that IDO inhibition may favour immune-mediated control of HIV replication [1,2]. Strategies interfering with the binding of CTLA-4 to its ligands B7.1 and B7.2 have shown ambiguous results, but the effect of CTLA-4 blockade may only be partially dependent on IDO suppression [3,4]. In addition, simultaneous administration of D-1mT and anti-CTLA-4 to Rhesus macaques caused fatal pancreatitis, calling for caution when considering strategies which may reverse immune tolerance [5]. Other therapeutic options aim at dampening the generalised immune activation by using compounds with broad anti-inflammatory properties, particularly those interfering with pDC activation, a notable example is that of the antimalaric drug chloroquine and its derivative hydroxychloroquine (CQ and hCQ). However, the direct effect of these compounds on IDO activity in vivo is yet to be determined. Thus, inhibition of IDO or IDO-related pathways may represent a valid therapeutic option in the setting of HIV infection, but its application is still limited by the paucity of specifically designed comparative preclinical and clinical studies.
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