Abstract
Infection with the human immunodeficiency virus type 1 (HIV) results in a chronic infection that progressively cripples the host immune defenses. HIV infection is associated with increased tryptophan (trp) catabolism by the cytokine-inducible enzyme indoleamine 2,3-dioxygenase (IDO). IDO has powerful immune suppressive activity, which could contribute to the immune dysfunction observed in HIV-infected patients. In this review we discuss the immune mechanisms that could mediate the HIV-induced increase of IDO activity (such as IFN-γ , IFN-α , CTLA-4/B7 and direct viral exposure). We then consider the current knowledge of IDO-mediated immune suppressive mechanisms with regard to different cell types (CD4+ T cells, CD8+ T cells, natural killer cells, B cells and regulatory T cells), from the perspective of their potential consequences for the HIV-infected host. HIV-induced, IDO-mediated trp catabolism may contribute to the perpetuation of HIV infection into its chronic phase by dampening efficient immune anti-viral responses. Therapeutic approaches aimed at manipulating this powerful immune suppressive mechanism might be considered in the setting of HIV infection.
Keywords: Indoleamine 2,3-dioxygenase, HIV, immune suppression
Current Drug Metabolism
Title: How Does Indoleamine 2,3-Dioxygenase Contribute to HIV-Mediated Immune Dysregulation
Volume: 8 Issue: 3
Author(s): Adriano Boasso and Gene M. Shearer
Affiliation:
Keywords: Indoleamine 2,3-dioxygenase, HIV, immune suppression
Abstract: Infection with the human immunodeficiency virus type 1 (HIV) results in a chronic infection that progressively cripples the host immune defenses. HIV infection is associated with increased tryptophan (trp) catabolism by the cytokine-inducible enzyme indoleamine 2,3-dioxygenase (IDO). IDO has powerful immune suppressive activity, which could contribute to the immune dysfunction observed in HIV-infected patients. In this review we discuss the immune mechanisms that could mediate the HIV-induced increase of IDO activity (such as IFN-γ , IFN-α , CTLA-4/B7 and direct viral exposure). We then consider the current knowledge of IDO-mediated immune suppressive mechanisms with regard to different cell types (CD4+ T cells, CD8+ T cells, natural killer cells, B cells and regulatory T cells), from the perspective of their potential consequences for the HIV-infected host. HIV-induced, IDO-mediated trp catabolism may contribute to the perpetuation of HIV infection into its chronic phase by dampening efficient immune anti-viral responses. Therapeutic approaches aimed at manipulating this powerful immune suppressive mechanism might be considered in the setting of HIV infection.
Export Options
About this article
Cite this article as:
Boasso Adriano and Shearer M. Gene, How Does Indoleamine 2,3-Dioxygenase Contribute to HIV-Mediated Immune Dysregulation, Current Drug Metabolism 2007; 8 (3) . https://dx.doi.org/10.2174/138920007780362527
DOI https://dx.doi.org/10.2174/138920007780362527 |
Print ISSN 1389-2002 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5453 |
- Author Guidelines
- Graphical Abstracts
- Fabricating and Stating False Information
- Research Misconduct
- Post Publication Discussions and Corrections
- Publishing Ethics and Rectitude
- Increase Visibility of Your Article
- Archiving Policies
- Peer Review Workflow
- Order Your Article Before Print
- Promote Your Article
- Manuscript Transfer Facility
- Editorial Policies
- Allegations from Whistleblowers
- Announcements
Related Articles
-
Natural Products Homoharringtonine and Emetine Alkaloids as SARS-CoV-2 Treatment Options
Current Pharmaceutical Design Molecular Imaging with Small Animal PET/CT
Current Medical Imaging Caring for HIV-Infected Patients in the ICU in The Highly Active Antiretroviral Therapy Era
Current HIV Research Dengue Virus RNA Polymerase NS5: A Potential Therapeutic Target?
Current Drug Targets Therapeutic Options in Prevention and Treatment of Aspartoacylase Gene Mutation Resulting Abnormalities in Canavan Disease
Current Pharmacogenomics Schistosoma mansoni Antigens as Modulators of the Allergic Inflammatory Response in Asthma
Endocrine, Metabolic & Immune Disorders - Drug Targets Acanthamoeba-Bacteria: A Model to Study Host Interaction with Human Pathogens
Current Drug Targets Novel Phospholipase-Resistant Lipid/Peptide Synthetic Lung Surfactants
Mini-Reviews in Medicinal Chemistry Neuroglobin and Estrogen Receptors: A New Pathway of Cell Survival and Cell Death Balance
Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry (Discontinued) PTD/CPP Peptide-Mediated Delivery of siRNAs
Current Pharmaceutical Design Viral Envelope Membrane: A Special Entry Pathway and a Promising Drug Target
Current Medicinal Chemistry Targeting Strategies in Therapeutic Applications of Toxoplasmosis: Recent Advances in Liposomal Vaccine Delivery Systems
Current Drug Targets Oncotarget Strategies For Herpes Simplex Virus-1
Current Gene Therapy Recent Updates on Development of Drug Molecules for Human African Trypanosomiasis
Current Topics in Medicinal Chemistry Medicinal Plants with anti-Acanthamoeba Activity: A Systematic Review
Infectious Disorders - Drug Targets Mechanisms of Neuronal Injury and Death in HIV-1 Associated Dementia
Current HIV Research Potential Factors Induced by Filoviruses that Lead to Immune Supression
Current Molecular Medicine DHODH Hot Spots: An Underexplored Source to Guide Drug Development Efforts
Current Topics in Medicinal Chemistry The Multiple Layers of Signaling Selectivity at Protease-Activated Receptors
Current Pharmaceutical Design Synthetic and Natural Protease Inhibitors Provide Insights into Parasite Development, Virulence and Pathogenesis
Current Medicinal Chemistry