Abstract
Progression from latency to active Tuberculosis (TB) disease is mediated by incompletely understood host immune factors. The definitive characteristic of progressive human immunodeficiency virus (HIV) disease is a severe loss in number and function of T lymphocytes. Among the many possible mediators of T lymphocyte loss and ineffective function is the activity of the immune-modulatory enzyme indoleamine 2,3-dioxygenase (IDO). IDO is the rate-limiting enzyme converting tryptophan to kynurenine. IDO activity was initially recognized to mediate tolerance at the foeto-maternal interface. Recently, IDO activity has also been noted to play a critical role in immune tolerance to pathogens. Studies of host immune and metabolic mediators have found IDO activity significantly elevated in HIV and TB disease. In this review, we explore the link between IDO-mediated tryptophan catabolism and the presence of active TB disease in HIV-infected patients. We draw attention to increased IDO activity as a key factor marking the progression from latent to active TB disease in HIV-infected patients.
Highlights
The effect of indoleamine 2,3-dioxygenase-1 (IDO) activity in various diseases, including tuberculosis (TB) and human immunodeficiency virus (HIV) disease has generated considerable interest
In the last three decades, a wealth of information has indicated that IDO activation and its associated metabolites play a role in human HIV infection and early progression to AIDS (Fuchs et al, 1990; Hunt et al, 2014; Jenabian et al, 2015; Mehraj and Routy, 2015; Gelpi et al, 2017)
We speculate that increased IDO-mediated tryptophan catabolism in HIV infection may be more than merely an association, but play a causal role in susceptibility to disease, active TB
Summary
The effect of indoleamine 2,3-dioxygenase-1 (IDO) activity in various diseases, including tuberculosis (TB) and human immunodeficiency virus (HIV) disease has generated considerable interest. Both HIV-infection and TB disease are associated with upregulation of IDO activity (Divanovic et al, 2011; Blumenthal et al, 2012; Chen et al, 2014). In the last three decades, a wealth of information has indicated that IDO activation and its associated metabolites play a role in human HIV infection and early progression to AIDS (Fuchs et al, 1990; Hunt et al, 2014; Jenabian et al, 2015; Mehraj and Routy, 2015; Gelpi et al, 2017). Werner et al (1988) reported that HIV-infected patients have high serum kynurenine-to-tryptophan ratio (IDO activity).
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