ReviewCellular and molecular life sciences : CMLS2018
The potential importance of myeloid-derived suppressor cells (MDSCs) in the pathogenesis of Alzheimer's disease.
Review in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Advances in immune cell-based therapeutic agents for the treatment of inflammation-related diseases.Acta pharmaceutica Sinica. B · 2026Review
- Mitochondrial dysfunction and programmed cell death in Alzheimer's disease: A retrospective bioinformatics study.Medicine · 2026Article
- The vasoprotective role of Myeloid-derived suppressor cells in pathogenesis of aortic dissection.Scientific reports · 2026Article
- Neuroimmune Mechanisms in Traumatic Brain Injury and Cancer: Parallel Courses or Existence in Different Orbits.Biomedicines · 2026Review
- FLOT1 and EEF1D: ac4C-related genes bridging Alzheimer's disease and sleep deprivation.Frontiers in aging neuroscience · 2026Article
- Establishment and Validation of the Diagnostic Value of Oligodendrocyterelated Genes in Alzheimer's Disease.CNS & neurological disorders drug targets · 2025Article
- The role of peripheral innate immune cells in Alzheimer's disease progression.Frontiers in immunology · 2025Review
- Integrative bioinformatics and machine learning identify iron metabolism genes MAP4, GPT, and HIRIP3 as diagnostic biomarkers and therapeutic targets in Alzheimer's disease.Frontiers in cellular neuroscience · 2025Article
- Alzheimer's disease following COVID-19: a two player match?Infection · 2024Article
- The effects of high plasma levels of AβImmunity & ageing : I & A · 2023Article
- Identification of TIMP1 as an inflammatory biomarker associated with temporal lobe epilepsy based on integrated bioinformatics and experimental analyses.Journal of neuroinflammation · 2023Article
- Article
- Neutrophils as a potential therapeutic target in Alzheimer's disease.Frontiers in immunology · 2023Review
- Identification of disulfidptosis-related genes and subgroups in Alzheimer's disease.Frontiers in aging neuroscience · 2023Article
- Systematic analysis of cuproptosis-related genes in immunological characterization and predictive drugs in Alzheimer's disease.Frontiers in aging neuroscience · 2023Article
- Eriodictyol and Homoeriodictyol Improve Memory Impairment in AβMolecules (Basel, Switzerland) · 2022Article
- In Situ Deployment of Engineered Extracellular Vesicles into the Tumor Niche via Myeloid-Derived Suppressor Cells.Advanced healthcare materials · 2022Article
- ER stress activates immunosuppressive network: implications for aging and Alzheimer's disease.Journal of molecular medicine (Berlin, Germany) · 2020Review
- Roles of Gut Microbiota in the Regulation of Hippocampal Plasticity, Inflammation, and Hippocampus-Dependent Behaviors.Frontiers in cellular and infection microbiology · 2020Review
- Functional alterations of myeloid cells during the course of Alzheimer's disease.Molecular neurodegeneration · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The exact cause of Alzheimer's disease (AD) is still unknown, but the deposition of amyloid-β (Aβ) plaques and chronic inflammation indicates that immune disturbances are involved in AD pathogenesis. Recent genetic studies have revealed that many candidate genes are expressed in both microglia and myeloid cells which infiltrate into the AD brains. Invading myeloid cells controls the functions of resident microglia in pathological conditions, such as AD pathology. AD is a neurologic disease with inflammatory component where the immune system is not able to eliminate the perpetrator, while, concurrently, it should prevent neuronal injuries induced by inflammation. Recent studies have indicated that AD brains are an immunosuppressive microenvironment, e.g., microglial cells are hyporesponsive to Aβ deposits and anti-inflammatory cytokines enhance Aβ deposition. Immunosuppression is a common element in pathological disorders involving chronic inflammation. Studies on cancer-associated inflammation have demonstrated that myeloid-derived suppressor cells (MDSCs) have a crucial role in the immune escape of tumor cells. Immunosuppression is not limited to tumors, since MDSCs can be recruited into chronically inflamed tissues where inflammatory mediators enhance the proliferation and activation of MDSCs. AD brains express a range of chemokines and cytokines which could recruit and expand MDSCs in inflamed AD brains and thus generate an immunosuppressive microenvironment. Several neuroinflammatory disorders, e.g., the early phase of AD pathology, have been associated with an increase in the level of circulating MDSCs. We will elucidate the immunosuppressive armament of MDSCs and present evidences in support of the crucial role of MDSCs in the pathogenesis of AD.
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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.