The role of the immune system in driving neuroinflammation
Open accessAbstract
Neuroinflammation is now recognised as an important contributory factor in the progression of Alzheimer’s disease and probably also in the early stages of the disease. It is likely that this derives largely from aberrant activation of microglia, the resident mononuclear phagocytes of the brain. These cells are responsible for physiological immune surveillance and clearance of pathogens in the central nervous system, but evidence indicates that in Alzheimer’s disease, microglial function is compromised, and this contributes to the pathology. It is unclear what factors cause the inappropriate activation of the microglia in Alzheimer’s disease, but one contributor may be infiltrating peripheral immune cells and these include macrophages and T cells. It has been suggested that both cell types modulate the phenotype of microglia, highlighting the importance of crosstalk between the innate and adaptive immune system in Alzheimer’s disease. This review outlines our current knowledge of how cells of the peripheral immune system, specifically macrophages and T cells, may modulate microglial phenotype in the context of Alzheimer’s disease and considers the impact on their function, especially phagocytic capacity.
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Some studies suggest that infiltrating macrophages possess a greater ability than resident microglia to remove CNS plaques.
“Some studies suggest that infiltrating macrophages possess a greater ability than resident microglia to remove CNS plaques,15–17”
From TET2-mutant myeloid cells mitigate Alzheimer’s disease progression via CNS infiltration and enhanced phagocytosis in mice (2025) · cites this paper as [15]
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- Authors
- Ní Chasaide, C., & Lynch, M. A.
- Affiliations
- Trinity College Institute for Neuroscience, Trinity College Dublin, Dublin, Ireland
- Trinity College Dublin (IE)
- Corresponding author
- Lynch, Marina A
- Venue
- Brain and Neuroscience Advances
- Publisher
- SAGE Publications
- Published
- 2020-01
- Volume
- 4
- Pages
- 239821281990108
- ISSN
- 2398-2128 (ISSN-L)
- PMC
- PMC7085916
- OpenAlex
- W3004066393
- Cited by
- 72
- References
- 24
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- gold
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- Lenus, The Irish Health Repository (Dr Steevens Hospital Library) (submittedVersion)
- Funders
- Science Foundation Ireland (15/iA/3052)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- neuroinflammation, Alzheimer's disease, microglia, microglial activation, macrophages, T cells, peripheral immune cells, innate-adaptive immune crosstalk, phagocytosis, microglial phenotype
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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