ReviewOpen biology2021
Myeloid-derived suppressor cells and the pathogenesis of human immunodeficiency virus infection.
Review in Open biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
The trial behind it
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
13 citing papers in PubMed, 16 citations in OpenAlex.
- Granulocytic myeloid-derived suppressor cells sustain HIV reservoirs by inhibiting viral reactivation via arginase 1-mediated mechanisms.JCI insight · 2026Article
- Myeloid-derived suppressor cells inhibit the replication of oncolytic virus by reducing intratumoral arginine levels.Molecular therapy. Oncology · 2025Article
- A role of arginase-1-expressing myeloid cells in cachexia.Cancer & metabolism · 2025Article
- HIV, Sepsis, and Postdischarge Mortality in Sub-Saharan Africa.American journal of respiratory and critical care medicine · 2025Article
- Editorial: HIV/AIDS: pathogenesis and vaccine.Frontiers in cellular and infection microbiology · 2025Article
- The role of myeloid-derived suppressor cells in children.Frontiers in pediatrics · 2025Review
- MDSC expansion during HIV infection: regulators, ART and immune reconstitution.Genes and immunity · 2024Review
- Polymorphonuclear myeloid-derived suppressor cells regulates immune recovery during HIV infection through PD-L1 and TGF-β pathways.Frontiers in cellular and infection microbiology · 2024Article
- The Role of p53 in HIV Infection.Current HIV/AIDS reports · 2023Review
- Recruitment of myeloid‑derived suppressor cells and regulatory T‑cells is associated with the occurrence of acute myocardial infarction.Biomedical reports · 2023Article
- Counteracting Immunosenescence-Which Therapeutic Strategies Are Promising?Biomolecules · 2023Review
- Major alterations to monocyte and dendritic cell subsets lasting more than 6 months after hospitalization for COVID-19.Frontiers in immunology · 2022Article
- New Discovery of Myeloid-Derived Suppressor Cell's Tale on Viral Infection and COVID-19.Frontiers in immunology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There are several mechanisms by which human immunodeficiency virus (HIV) can mediate immune dysfunction and exhaustion during the course of infection. Chronic immune activation, after HIV infection, seems to be a key driving force of such unwanted consequences, which in turn worsens the pathological status. In such cases, the immune system is programmed to initiate responses that counteract unwanted immune activation, for example through the expansion of myeloid-derived suppressor cells (MDSCs). Although the expansion of immune suppressor cells in the setting of systemic chronic immune activation, in theory, is expected to contain immune activation, HIV infection is still associated with a remarkably high level of biomarkers of immune activation. Paradoxically, the expansion of immune suppressor cells during HIV infection can suppress potent anti-viral immune responses, which in turn contribute to viral persistence and disease progression. This indicates that HIV hijacks not only immune activation but also the immune regulatory responses to its advantage. In this work, we aim to pave the way to comprehend how such unwanted expansion of MDSCs could participate in the pathology of acute/primary and chronic HIV infection in humans, as well as simian immunodeficiency virus infection in rhesus macaques, according to the available literature.
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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.