ReviewJournal of leukocyte biology2019
Contribution of IDO to human respiratory syncytial virus infection.
Review in Journal of leukocyte biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Severe Hospitalization-Requiring Viral Infection With Influenza or COVID-19: Metabolic Pathway Analysis.Open forum infectious diseases · 2026Article
- Multi-omic spatial profiling reveals the unique SARS-CoV-2 lung microenvironment and collagen VI as a predictive biomarker in severe COVID-19.The European respiratory journal · 2025Article
- Amino acid catabolite markers for early prognostication of pneumonia in patients with COVID-19.Nature communications · 2023Article
- Blockade of Indoleamine 2,3-Dioxygenase attenuates lipopolysaccharide-induced kidney injury by inhibiting TLR4/NF-κB signaling.Clinical and experimental nephrology · 2023Article
- Clinical, radiological and pathological findings in patients with persistent lung disease following SARS-CoV-2 infection.The European respiratory journal · 2022Article
- Covid-19 Interstitial Pneumonia: Histological and Immunohistochemical Features on Cryobiopsies.Respiration; international review of thoracic diseases · 2021Article
- Indoleamine 2,3-Dioxygenase Is Involved in Interferon Gamma's Anti-BKPyV Activity in Renal Cells.Viruses · 2020Article
- AhR and IDO1 in pathogenesis of Covid-19 and the "Systemic AhR Activation Syndrome:" a translational review and therapeutic perspectives.Restorative neurology and neuroscience · 2020Review
- Contribution of IDO to human respiratory syncytial virus infection.Journal of leukocyte biology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IDO is an enzyme that participates in the degradation of tryptophan (Trp), which is an essential amino acid necessary for vital cellular processes. The degradation of Trp and the metabolites generated by the enzymatic activity of IDO can have immunomodulating effects, notably over T cells, which are particularly sensitive to the absence of Trp and leads to the inhibition of T cell activation, cell death, and the suppression of T cell effector functions. Noteworthy, T cells participate in the cellular immune response against the human respiratory syncytial virus (hRSV) and are essential for viral clearance, as well as the total recovery of the host. Furthermore, inadequate or non-optimal polarization of T cells is often seen during the acute phase of the disease caused by this pathogen. Here, we discuss the capacity of hRSV to exploit the immunosuppressive features of IDO to reduce T cell function, thus acquiring relevant aspects during the biology of the virus. Additionally, we review studies on the influence of IDO over T cell activation and its relationship with hRSV infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.