MicroRNA-125b Potentiates Macrophage Activation
Open accessAbstract
MicroRNA (miR)-125b expression is modulated in macrophages in response to stimulatory cues. In this study, we report a functional role of miR-125b in macrophages. We found that miR-125b is enriched in macrophages compared with lymphoid cells and whole immune tissues. Enforced expression of miR-125b drives macrophages to adapt an activated morphology that is accompanied by increased costimulatory factor expression and elevated responsiveness to IFN-γ, whereas anti-miR-125b treatment decreases CD80 surface expression. To determine whether these alterations in cell signaling, gene expression, and morphology have functional consequences, we examined the ability of macrophages with enhanced miR-125b expression to present Ags and found that they better stimulate T cell activation than control macrophages. Further indicating increased function, these macrophages were more effective at killing EL4 tumor cells in vitro and in vivo. Moreover, miR-125b repressed IFN regulatory factor 4 (IRF4), and IRF4 knockdown in macrophages mimicked the miR-125b overexpression phenotype. In summary, our evidence suggests that miR-125b is at least partly responsible for generating the activated nature of macrophages, at least partially by reducing IRF4 levels, and potentiates the functional role of macrophages in inducing immune responses.
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miR-125b represses IRF4 and induces CD80 expression, enhancing macrophage antigen-presenting capacity.
“Chaudhuri et al. demonstrated that miR-125b represses IFN regulatory factor 4 (IRF4) and induces CD80 expression, which enhances macrophage antigen presenting cells’ capacities [143].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [143]
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- Authors
- Chaudhuri, A. A., So, A. Y.-L., Sinha, N., Gibson, W. S. J., Taganov, K. D., O’Connell, R. M., & Baltimore, D.
- Affiliations
- California Institute of Technology (US)
- Regulus Therapeutics (United States) (US)
- University of Utah (US)
- Corresponding author
- Sinha, Nikita
- Baltimore, David
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-11
- Volume
- 187
- Issue
- 10
- Pages
- 5062-5068
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC3208133
- OpenAlex
- W2115048931
- Cited by
- 327
- References
- 35
- Citations by year
- 2026: 6 · 2025: 19 · 2024: 14 · 2023: 23 · 2022: 21 · 2021: 26 · 2020: 29 · 2019: 29 · 2018: 20 · 2017: 23 · 2016: 27 · 2015: 25 · 2014: 25 · 2013: 29 · 2012: 10
- FWCI
- 6.97
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (K99HL102228)
- National Cancer Institute (F32CA139883)
- National Institute of Allergy and Infectious Diseases (R01AI079243)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- miR-125b, macrophage activation, IRF4, antigen presentation, T cell activation, tumor cell killing, macrophage morphology
- MeSH terms
- Animals, Base Sequence, Bone Marrow Cells, Cell Line, Cytotoxicity Tests, Immunologic, Humans, Lymphocyte Activation, Macrophage Activation, Macrophages, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Transgenic, Molecular Sequence Data, Spleen, Thymus Gland, T-Lymphocyte Subsets, Antigen Presentation, Coculture Techniques, MicroRNAs, Cell Line, Tumor, Mice, HEK293 Cells
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