The DOI matches its Crossref record; 48 of the 48 references it cites were found in a registry or an index.
miR‐155 as a multiple sclerosis–relevant regulator of myeloid cell polarization
Open accessAbstract
Objective: To define the functional significance of increased miR‐155 expression in myeloid cells in multiple sclerosis (MS). Methods: miR‐155 expression levels were measured in CD14 + monocytes from untreated relapsing–remitting MS patients and compared to healthy controls. Similar microRNA (miRNA) analyses were performed in laser‐captured CD68 + cells from perivascular (blood‐derived macrophages) and parenchymal (microglia) brain regions in both active MS lesions and noninflammatory cases. Using human adult blood‐derived macrophages and brain‐derived microglia, in vitro experiments were performed to demonstrate how miR‐155 influences the polarization state, phenotype, and functional properties of myeloid cells, in addition to their ability to subsequently impact adaptive T‐cell responses. Results: In MS, miR‐155 expression was significantly increased in both peripheral circulating CD14 + monocytes and active lesions (CD68 + cells) compared to control donor monocytes and parenchymal microglia, respectively. In vitro, miR‐155 was significantly increased in both M1‐polarized primary human macrophages and microglia. Transfection of an miR‐155 mimic increased proinflammatory cytokine secretion and costimulatory surface marker expression in both cell types; an miR‐155 inhibitor decreased proinflammatory cytokine expression. Coculture experiments demonstrated that allogeneic T‐cell responses were significantly enhanced in the presence of miR‐155–transfected myeloid cells compared to controls. Interpretation: Our results demonstrate that miR‐155 regulates proinflammatory responses in both blood‐derived and central nervous system (CNS)‐resident myeloid cells, in addition to impacting subsequent adaptive immune responses. Differential miRNA expression may therefore provide insight into mechanisms responsible for distinct phenotypic and functional properties of myeloid cells, thus impacting their ability to influence CNS injury and repair. Ann Neurol 2013;74:709–720
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“Also, since many disorders share the same proteins or micro RNAs as markers, it is impossible to have selective detection of diseases [313–317].”
From Extracellular vesicles as nanotheranostic platforms for targeted neurological disorder interventions (2024) · cites this paper as [314]
In the citing paper
“MiR-155 is upregulated in M1-polarized macrophages and microglia, and in those cells in patients with multiple sclerosis [248].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [248]
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“It is upregulated in active lesions, PBMCs and CD14+ monocytes [42,43], is induced in brain endothelium where it disrupts BBB integrity and promotes leukocyte adhesion [26,44], drives Th1/Th17 differentiation and pro-inflammatory myeloid polarization [45,46], and its genetic deletion or silencing…”
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“Elevated miR-155 expression has also been noted in brain lesions and CD14 + cells of MS patients [28 ].”
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“These monocytes further promote the upregulation of miR-155 (9) and the co-stimulatory molecule CD80, thereby amplifying T-cell-mediated inflammatory responses.”
Vrînceanu, O., Maier, S., Manu, D. R., Bănescu, C. V., & Bălașa, R. (2026) · Cells · doi:10.3390/cells15161441
“…with established roles in destabilising endothelial tight junction proteins and thereby contributing to BBB permeability under inflammatory conditions [20], as well as in promoting a pro-inflammatory myeloid cell phenotype and regulating Th1/Th17 T lymphocyte differentiation (Figure 10) [21–23].”
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“…involved in remyelination: miRNA-155 and miR-223. miR-155 is a proinflammatory miRNA, being relevant in myeloid cell polarization in MS (Hu et al., 2022; Moore et al., 2013) and in LPS-treated BV2 cells; miR-155 increases the release of the pro-inflammatory cytokine IL1 β (Yin et al., 2017).”
Metadata
- Authors
- Moore, C. S., Rao, V. T. S., Durafourt, B. A., Bedell, B. J., Ludwin, S. K., Bar‐Or, A., & Antel, J. P.
- Affiliations
- Montreal Neurological Institute and Hospital (CA)
- Queen's University (CA)
- Corresponding author
- Moore, Craig S.
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2013-09-23
- Volume
- 74
- Issue
- 5
- Pages
- 709-720
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- OpenAlex
- W1915908724
- Cited by
- 219
- References
- 48
- Citations by year
- 2026: 8 · 2025: 6 · 2024: 13 · 2023: 11 · 2022: 13 · 2021: 15 · 2020: 25 · 2019: 26 · 2018: 23 · 2017: 24 · 2016: 23 · 2015: 15 · 2014: 15 · 2013: 2
- FWCI
- 13.71
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- miR-155, multiple sclerosis, myeloid cell polarization, microglia, blood-derived macrophages, CD14+ monocytes, M1 macrophage polarization, inflammatory cytokines, costimulatory molecules, T cell response, relapsing-remitting multiple sclerosis, neuroinflammation
- MeSH terms
- Adult, Aged, Brain, Female, Humans, Macrophages, Male, Middle Aged, Multiple Sclerosis, T-Lymphocytes, Cell Polarity, Microglia, Myeloid Cells, MicroRNAs, Cell Proliferation, Adaptive Immunity
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